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SYNOPSIS  OF  LECTURES 


UPON 


Diseases  of  the  Nervous  System 


BY 

PROF.  M.  ALLEN   STARR 


COLLEGE  OF  PHYSICIANS  AND  SURGEONS 
MEDICAL  DEPARTMENT  OF  COLUMBIA  COLLEGE 


NEW   YORK 

TROW   DIRECTORY,   PRINTING   AND   BOOKBINDING   CO. 

201-213  EAST  TWELFTH  STREET 

1894 


COPYRIGHT,  1893,  BY 
M.   ALLEN    STARR 


WL 

loo 


SYNOPSIS   OF   LECTURES 

UPON 

DISEASES    OF   THE   NERVOUS    SYSTEM. 


A  KNOWLEDGE  of  the  structure  and  functions  of  the  central 
nervous  system  is  an  essential  preliminary  to  the  study  of  its  dis- 
eases. The  human  nervous  system  is  the  most  complex  of  all 
nervous  structures,  and  is  the  culmination  of  the  process  of  evo- 
lution It  will  aid  in  the  understanding  of  its  structure  if  the 
various  stages  in  its  evolution  are  known. 

THE  EVOLUTION  OF  THE    NERVOUS  SYSTEM. 

The  simplest  form  of  a  nervous  system  consists  of  a  single 
mass  of  gray  matter  with  a  sensory  and  a  motor  nerve. 

The  mass  of  gray  matter  receives  impulses  sent  from  the  sur- 
face by  the  sensory  fibre,  acts  in  response  to  the  impulse,  and 
the  action  is  transmitted  to  a  motor  mechanism  by  the  motor 
nerve. 

Example.  The  closure  of  an  oyster-shell  when  the  oyster  feels 
any  object  touching  its  sensory  surface.  Parallel  action  in  hu- 
man system — any  spinal  reflex — e.g.,  knee-jerk. 

Several  such  single  masses  may  be  joined  to  one  another, 
each  with  its  sensory  and  motor  nerve.  The  masses  receive  im- 
pulses in  succession  and  act  in  succession. 

Example.     Wave-like  motion  of  a  jelly-fish  or  caterpillar. 

A  compound  type  of  nervous  system  consists  of  several  sub- 
ordinate masses  joined  together  and  presided  over  by  a  single 
higher  mass,  which  is  joined  to  each  of  the  lower  masses.  The 
higher  mass  receives  impulses  from  the  lower  masses,  not  di- 
rectly from  the  surface.  It  sends  impulses  to  the  motor  mech- 
anisms through  the  lower  masses,  not  directly.  It  secures  a  cer- 


4  DISEASES   OF   THE   NERVOUS   SYSTEM. 

tain  definite  succession  and  combination  of  action  in  the  lower 
masses. 

Examples.  The  nervous  system  of  a  frog  experimentally  de- 
prived of  its  hemispheres,  capable  of  automatic  acts  of  swim- 
ming. The  automatic  act  of  respiration  in  man.  In  man  the 
facial,  laryngeal,  intercostal,  thoracic,  and  diaphragmatic  respira- 
tory muscles  act  in  definite  succession  and  rhythm  in  the  act  of 
breathing  ;  and  this  act  is  presided  over  by  a  single  centre  in  the 
medulla  controlling  the  lower  medullary  and  spinal  centres. 

The  highest  type  of  nervous  system  is  the  complex  type. 
There  are  the  lower  centres  as  in  the  simple  type.  There  are 
higher  centres  controlling  the  lower  centres,  as  in  the  compound 
type.  There  is  a  supreme  mass  controlling  both  the  others. 

This  is  the  form  found  in  all  vertebrates,  and  the  degree  of 
evolution  in  the  highest  or  supreme  mass  determines  the  place 
of  the  animal  in  the  scale  of  intelligence. 

In  man  the  supreme  mass  is  the  cerebral  cortex,  the  next 
lower  or  automatic  centres  are  the  optic  thalami  and  basal  gan- 
glia, including  gray  masses  in  the  cerebral  ax*is  ;  the  lowest  or 
reflex  centres  are  the  cranial  nerve  nuclei  in  the  cerebral  axis  and 
the  gray  matter  of  the  spinal  cord  segments. 

These  distant  gray  masses  are  joined  with  one  another  in  all 
possible  combinations  by  means  of  the  \vhite  nerve  tracts,  which 
pass  in  all  directions  around  and  within  them. 

Read  Herbert  Spencer,  "  Principles  of  Psychology,"  Part  I.,  Chaps.  I. -IV. 
Charles  Mercier,  "The  Nervous  System  and  the  Mind,"  Part  I. 

THE  HUMAN  NERVOUS  SYSTEM. 

The  human  nervous  system  consists  of  a  peripheral  system 
and  a  central  system. 

The  peripheral  system  comprises  all  the  nerves. 

The  central  system  includes  : 

First.  The  spinal  cord  and  cranial  nerve  nuclei. 

Secondly.  The  cerebellum  ;  gray  masses  of  the  medulla,  pons, 
and  crura  cerebri ;  corpora  quadrigemina,  optic  thalami,  and  cor- 
pora striata. 

Thirdly.  The  cerebral  cortex. 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


THE    PERIPHERAL   NERVES   AND    THEIR   DISEASES. 


STRUCTURE  of  the  nerves.  Bundles  of  nerve  fibres — large  or 
small. 

Structure  of  a  nerve  fibre  :  i.  Axis  cylinder,  a  long  process 
of  some  nerve  cell.  2.  Medullary  sheath  of  myelin — a  fatty  in- 
sulator, interrupted  at  the  nodes  of  Ranvier.  3.  Connective 
tissue  sheath  of  Schwann,  with  its  nucleus.  Nerve  fibres  are 
bound  into  bundles  by  connective  tissue  ;  endoneurium,  peri- 
neurium.  The  visceral  nerve  fibres  have  no  medullary  sheath. 

All  nerve  fibres  branch  during  their  course  in  the  central 
nervous  system,  sending  out  "collaterals,"  but  do  not  branch  in 
their  peripheral  course.  They  arise  from  a  nerve  cell.  They 
terminate  in  fine  brush-like  expansions  which  are  spread  out  in 
the  skin,  or  on  a  muscle,  or  around  another  nerve  cell. 

Nerves  are  divided  into  motor  nerves  and  sensory  nerves,  ac- 
cording to  the  mechanism  to  which  they  are  attached.  Motor 
nerves  convey  impulses  outward,  sensory  inward.  Motor  nerves 
grow  outward  from  large  nerve  cells  in  the  spinal  cord.  Sen- 
sory nerves  grow  from  cells  in  the  posterior  spinal  ganglia,  which 
send  one  branch  to  the  surface,  and  the  other  into  the  spinal 
cord. 

NEURITIS. 

Neuritis  may  occur  in  a  single  nerve,  or  in  a  plexus. 

Causes. — Injuries,  strains,  pressure,  compression  in  fractures, 
rheumatism,  gout,  cold. 

Pathology. — i.  Parenchymatous  neuritis,  congestion  and  exu- 
dation in  nerve- trunk  ;  swelling  and  degeneration  of  individual 
fibres  ;  i,  axis  cylinder  broken  and  disintegrated  in  fatty  mass  ; 
2,  medullary  substance  separated  into  segments  and  fatty  globules, 
and  mingled  with  granules  and  nucleated  cells  ;  3,  connective 
tissue  sheath  shrunken  and  empty.  Nuclei  multiply.  Products 
of  degeneration  liquefy  and  are  absorbed. 


6  DISEASES   OF   THE   NERVOUS   SYSTEM. 

Regeneration  occurs  by  growth  of  new  fibres  outward  from 
the  healthy  stump  into  the  old  sheath. 

2.  Interstitial  neuritis.  The  connective  tissue  of  the  endo- 
neurium  and  perineurium  increases  in  volume  and  the  nerve- 
fibres  are  compressed  by  the  congested  vessels  and  by  the  new 
tissue.  These  forms  usually  occur  together  in  non-traumatic 
cases. 

Symptoms. — Weakness  or  paralysis  with  atrophy  and  reaction  of 
degeneration  in  muscles  supplied  by  nerves  involved.  Reaction 
of  degeneration  (R.  D.)  is  a  change  in  the  action  of  the  nerves  and 
muscles  to  the  electric  currents.  The  response  of  the  nerve  to 
both  currents  is  lost.  The  muscle  loses  its  faradic  reaction.  The 
galvanic  reaction  is  changed,  the  muscle  responding  more  actively 
to  the  closure  of  the  positive  pole  (anode)  than  to  that  of  the 
negative  pole  (kathode).  Numbness  or  anaesthesia  in  skin  sup- 
plied by  nerve  involved.  Vasomotor  and  trophic  changes  in  the 
distribution  of  nerve  involved.  Coldness  from  sluggish  meta- 
bolism ;  glossy  skin;  oedema  ;  pain  and  tenderness  at  seat  of  in- 
flammation in  interstitial  cases. 

Course. — Slow  spontaneous  recovery  when  continuity  of  nerve 
is  preserved.  Otherwise,  no  recovery. 

Treatment. — If  nerve  is  broken  unite  divided  ends.  Rest  the 
part  injured  but  exercise  the  muscles  paralyzed  by  electricity 
and  massage.  Use  hot  applications,  sedative  lotions.  Protect 
from  cold  by  cotton  batting.  Morphine  for  pain. 

MULTIPLE  NEURITIS. 

Multiple  neuritis  is  an  inflammatory  or  degenerative  disease 
of  the  peripheral  nervous  system  varying  in  extent  and  inten- 
sity and  affecting  symmetrical  parts  of  the  body. 

The  motor  nerves  may  be  involved  alone  (e.g.,  in  lead  and 
mercury  poisoning),  or  the  sensory  nerves  alone  (e.g.,  in  coal-gas 
poisoning),  or  both  .may  be  involved  together  (e.g.,  in  alcoholic 
neuritis).  The  distal  parts  of  the  nerves  are  commonly  affected 
to  a  greater  extent  than  the  central  parts.  Hence  the  symptoms 
appear  chiefly  in  the  distal  parts  of  the  extremities. 

The  pathological  process  is  the  same  as  in  simple  neuritis  and 
may  be  parenchymatous  alone,  or  interstitial  alone,  or  both. 

Etiology. — i.  Toxic  cases  :  Alcohol,  lead,  arsenic,  bisulphide 
of  carbon,  copper,  zinc,  mercury,  phosphorus,  coal  gas. 


DISEASES   OF   THE   NERVOUS   SYSTEM.  7 

2.  Infectious  cases :  Diphtheria,  typhoid,  scarlet  fever,  measles, 
malaria,  leprosy,  beri  beri,  grippe. 

3.  Rheumatic  cases  :  Exposure  to  cold,  over-exertion. 

4.  Secondary   to   anaemia,  tuberculosis,  syphilis,  septicaemia, 
general  malnutrition,  and  diabetes. 

Symptoms. — Acute  or  sub-acute  onset  with  fever,  io3°-io4°  F., 
and  general  febrile  symptoms — sometimes  without  fever. 

Sensory  Symptoms. — First  to  occur.  Pain — Sharp,  severe,  lo- 
cated in  limbs,  increased  by  motion  or  pressure  ;  muscular  and 
nerve  tenderness,  sensitiveness. 

Paraesthesiae — Burning,  tingling,  numbness,  band  about  legs 
and  body. 

Anaesthesia — In  tips  of  fingers  and  toes,  extends  up  limbs. 

Ataxia — In  fine  movements  and  loss  of  sense  of  position. 

Motor  Symptoms. — Paralysis.  In  extensors,  dropped  wrist  and 
foot,  general  inability  to  walk  or  move  in  bed  ;  contractures  ; 
cranial  nerves  may  be  paralyzed  causing  symptoms  in  face. 

Atrophy — Rapid  in  onset.  R.  D.,  or  diminution  in  electric 
contractility  ;  loss  of  deep  reflexes  ;  no  paralysis  of  sphincters. 

Trophic  Symptoms. — Vasomotor  paralysis  ;  glossy  skin  ;  oedema  ; 
abnormal  growth  of  nails  and  hair  ;  sweating  profuse  ;  no  bed- 
sores ;  urticaria. 

Certain  cases  present  peculiar  features  in  their  course. 

1.  Alcoholic  Neuritis. — (a)  Rapid  onset  is  the  rule,  with  delirium 
and  delusions,  subsequently  imperfect  memory  of  recent  events. 
Total  paralysis,  with  very  great  pain  ;  anaesthesia  very  marked, 
also  tremor  and  tenderness  ;  dropped  wrists  and  feet  ;  or  (b)  All 
symptoms  of  locomotor   ataxia  develop  rapidly,  except  bladder 
and   rectal  loss    of  control.      In   both  forms  there  is  danger   of 
heart  failure    or   death    from    exhaustion,  due    to    complicating 
gastritis.      Usually    there    is,  rapid    increase    of    symptoms   for 
three  or  four  weeks,  and  then,  after  a  stationary  period  of  two 
months,  a  slow  progress  to  recovery,  the  duration  being  from  six 
to  twelve  months. 

2.  Lead  Neuritis. — Onset   with   intestinal   colic,  lead    line   on 
gums.     Paralysis  without  sensory  disturbance  in  hands,  causing 
dropped  wrists.     May  affect  all  muscles  of  arms  and  legs,  and  go 
on  to  sensory  symptoms  with  delusions,  but  this  is  rare. 

Gradual  recovery,  when  poison  is  eliminated,  in  four  months. 

3.  Arsenical  Cases.  —  Gastric    disturbance    at    outset.      Then 
paralysis  with  ataxia,  tremor,  atrophy,  and  great  numbness,  but 


8  DISEASES   OF   THE   NERVOUS   SYSTEM. 

little  pain  ;  legs  and  arms  equally  affected.     Recovery  in  two  to 
six  months,  depending  on  original  severity. 

4.  Coal   Gas    Cases.  —  Subacute   and   slight,    chiefly   sensory, 
numbness  for  a  long  time  in  fingers,  hands,  and  feet. 

5.  Diphtheritic   Cases.  —  Severe    paralysis    of    all   extremities, 
usually  without   sensory  disturbance,  cranial  nerves  frequently 
affected.     It  begins  in  uvula,  and  swallowing  and  talking  become 
difficult.    Eyes  are  often  turned.     Ataxia  is  marked  in  some  cases. 
Never  pain.     Progress  to  recovery  usual  in  three  months. 

6.  Epidemic  Form.     (Beri  beri.)     Occurs  in   Brazil,  Red  Sea, 
India,  Borneo.  Japan.     Several  types  :  acute  pernicious,  chronic 
cedematous,  chronic  atrophic.     Too  rare  to  need  attention  here. 
(See  Gowers,  L,  151  ;  also  New  York  Medical  Record,  February 
12,  1887.) 

Diagnosis. — From  anterior  poliomyelitis  :  by  pain,  tenderness 
along  nerves,  sensory  symptoms,  distribution  of  paralysis  sym- 
metrically. From  locomotor  ataxia :  by  rapid  onset  and 
paralysis,  preservation  of  control  of  bladder,  and  absence  of 
Argyle  Robertson  pupil.  From  myelitis  :  by  absence  of  affec- 
tion of  bladder  and  rectum,  by  absence  of  bed-sores,  and  tender- 
ness of  spine  to  heat,  and  by  distribution  of  symptoms  in  periph- 
ery. 

Prognosis. — Good  in  large  majority  of  cases;  slow  recovery ; 
bad  when  heart  becomes  rapid  and  respiration  poor. 

Treatment. — Rest  in  bed.  Warm  applications  by  packs  to 
limbs.  Rubbing  with  oil ;  gentle  massage  if  possible.  Prevent 
deformities  and  contractures  by  proper  position  of  limbs.  Elec- 
tricity, galvanism  through  nerves  and  to  muscles  after  acute  stage. 
Baths,  warm,  98°  F.,  for  half  hour  several  times  daily. 

Attention  to  diet,  nourish  well,  cut  off  alcohol  in  all  cases. 

General  and  nerve  tonics ;  iron,  quinine,  strychnine. 

In  acute  stage,  sodium  salicylate,  gr.  x.,  q.  3  hr.,  and  seda- 
tives, morphine,  phenacetine. 

In  chronic  stage,  arsenic  -fa  gr.  t.i.d.,  cod  liver  oil. 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


THE  SPINAL  CORD   AND   CRANIAL  NERVE  NUCLEI. 


THE  spinal  cord  in  man  is  made  up  of  thirty-one  segments — 
each  of  which  consists  of  a  mass  of  gray  matter  joined  to  a  pair 
of  spinal  nerves.  There  is  no  apparent  line  of  boundary  between 
adjacent  segments,  the  cord  being  a  long  cylindrical  organ.  But 
in  snakes  and  rabbits  the  area  of  gray  matter  is  much  larger 
opposite  the  entrance  of  nerves  than  between  them,  and  in  fishes 
there  is  a  visible  boundary  between  adjacent  segments. 

Each  segment  presents  a  symmetrical  arrangement  of  its 
two  halves.  Each  half  consists  of  a  central  collection  of  gray 
matter  surrounded  by  white  tracts.  Each  gray  mass  has  an  an- 
terior horn,  a  central  mass,  and  a  posterior  horn.  To  each  horn 
nerve  fibres  are  joined  making  the  anterior  and  posterior  nerve 
roots.  The  two  halves  are  separated  from  one  another  in  front 
by  the  anterior  fissure,  and  behind  by  the  posterior  septum. 
They  are  joined  together  by  the  anterior  white  commissure  and  by 
the  gray  commissure  in  which  lies  the  central  canal  of  the  cord. 
The  functions  of  each  segment  are  shown  in  the  table  on  page  10. 

THE  ANTERIOR  HORNS  OF  THE  SPINAL  CORD. 

These  vary  greatly  in  size  and  shape  in  various  segments, 
being  large  opposite  the  entrance  of  the  cervical  and  lumbo- 
sacral  nerves  and  thus  causing  the  cervical  and  lumbo-sacral 
enlargements  of  the  cord. 

,  Their  size  and  shape  depend  upon  the  number  of  groups  of 
cells  found  at  different  levels  ;  for  the  horns  are  made  up  of  cells 
— large,  polygonal  cells  with  nucleus  and  nucleolus — collected 
into  distinct  groups. 

Some  groups  of  cells  lie  on  the  edge  of  the  horn,  making 
projections  of  the  gray  mass  into  the  white  columns.  These 
groups  are  found  in  all  the  higher  vertebrates  and  are  not  pecul- 
iar to  man.  Other  groups  lie  within  the  horn  and  these  are 


10 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


Segment. 

Muscles. 

Reflex. 

Sensation. 

zd  and  3d  Cer- 

Sterno  mastoii       Tra- 

Hypochondrmm  (?)                       Back  of  head  to  vertex. 

vical. 

pezius. 

Sudden  inspiration   produced     Neck. 

Scaleni  and  neck. 

by  sudden  pressure  beneath 

Diaphragm. 

the  lower  border  of  ribs. 

4th  Cervical. 

Diaphragm. 

Pupil  4-7  cervical.                         Neck. 

Deltoid. 

Dilatation    of   the  pupil  pro-  '•  Upper  shoulder. 

Biceps.  Coraco-brachialis 

duced  by  irritation  of  neck.       Outer  arm. 

Supinator  Longus. 

Rhomboid. 

Supra  &  infra  spinatus. 

5th  Cervical. 

Deltoid. 

Scapular. 

Back  of  shoulder  and  arm. 

Biceps  Coraco-brachialis 

5th  Cervical  to  ist  Dorsal.            Outer  side  of  arm  and  fore- 

Brachialis  anticus. 

Irritation  of  skin  over  thescap-        arm. 

Supinator  longus. 

ula  produces  contraction  of 

Anterior  upper   two-thirds 

Supinator  brevis. 

the  scapular  muscles. 

of  arm. 

Deep  muscles  of  shoul- 

der blade. 

Supinator  Longus. 

Rhomboid.  Teres  minor.!  Tapping  its  tendon  in  wrist  pro- 

Pectoralis  (clav.  part). 

duces  flexion  of  forearm. 

Serratus  magnus. 

6th  Cervical. 

Brach.  anticus. 

Triceps. 

Outer  side  of  arm  and  fore- 

Pectoralis (clav.  part). 

5th  to  6th  Cervical. 

arm. 

Serratus  magnus. 

Tapping  elbow  tendon  produ- 

Inside  and  front  of  fore- 

Triceps. 

ces  extension  of  forearm. 

arm. 

Extensors  of  wrist  and 

fingers. 

Posterior  wrist. 

Pronators. 

6th  to  Sth  Cervical. 

Tapping    teudons  causes  ex- 

tension of  hand. 

7th  Cervical. 

Triceps  (long  head). 

Inner  and  back  of  arm  and 

Extensors  of  wrist  and 

forearm. 

fingers. 

Anterior  wrist. 

Pronators  of  wrist. 

7th-8th  Cervical. 

Radial  distribution  in  the 

Flexors  of  wrist. 

Tapping  anterior  tendon  causes 

hand. 

Subscapular. 

flexion  of  wrist. 

Pectoralis  (costal  part). 

Palmar.   ?th  Cerv.-  ist  Dorsal. 

Latissimus  dorsi. 

Stroking  palm  causes  closure 

Teres  major. 

of  fingers. 

8th  Cervical. 

Flexors    of   wrist    and 

Forearm  and  hand:  median 

fingers. 

and  ulnar  areas. 

Intrisic  muscles  of  hand. 

ist  Dorsal. 

Extensors  of  thumb. 

Ulnar  distribution  to  hand. 

Intrinsic  hand  muscles. 

Thenar  and  hypothenar 

eminences. 

zd    and    izth 

Muscles  of  back  and  ab- 

Epigastric.    4th-7th  Dorsal.        Skin  of  chest  and  abdomen, 

Dorsal. 

domen. 
Erectores  spins. 

in  bands  running  around 
Tickl'g  mammary  region  causes      and      downward     corre- 

retraction  of  the  epigastrium.      spending  to  spinal  nerves. 

Abdominal,     7th-  nth  Dorsal. 

Stroking  side  of  abdomen  caus-   Upper  eluteal  region. 

es  retraction  of  belly. 

ist  Lumbar. 

Ilio-psoas. 

Cremasteric.     ist~3d  Lumbar. 

Skin  over  groin  and  front 

Sartorius. 

Stroking   inner    thigh    causes         of  scrotum,  and  narrow 

retraction  of  scrotum.                     band  down  front  of  the 

zd  Lumbar. 

Ilio-psoas.     Sartorius. 

Patella  tendon. 

thigh  and  leg. 
Inner  side  of  thigh. 

Flexors  of  knee(  Remak). 
Quadriceps  femoris. 

Striking  tendon  causes  exten- 
sion of  leg.    2d-4th  Lumbar. 

Outer  side  of  thigh. 

3d  Lumbar. 

Quadriceps  femoris. 

Inner  rotators  of  thigh. 
Abductors  of  thigh. 

Inner  side  of  thigh  and  leg 
to  ankle. 

4th  Lumbar. 

Abductors  of  thigh. 

Gluteal. 

Inner  side  of  foot. 

Adductors  of  thigh. 

4th-5th  Lumbar. 

Flexors  of  knee  (Kerrier), 
Tibialis  anticus. 

Stroking  buttock  causes  dimpl- 
ing in  fold  of  buttock. 

5th  Lumbar. 

Outward     rotators     of 
thigh. 

Achilles  tendon. 
Over  extension  causes   rapid 

Lower  gluteal  region  back 
of  thigh.      Leg  and  foot 

Flexors  of  knee  (Ferrier). 
Flexors  of  ankle.  Peronei. 

flexion  of  ankle,  called  ankle 
clonus. 

outer  part. 

Extensors  of  toes. 

tst    and    id 

Flexors  of  ankle. 

Plantar. 

Leg  and  foot  except  inner 

Sacral. 

I-ong  flexor  of  toes. 
Intnnsic  muscles  of  foot. 

Tickling    sole    of    foot  causes 
flexion  of  toes  and  retraction 

side. 

of  leg. 

3d  to  sth  Sao   Peroneus  longus. 

Bladder  and  rectal  centre. 

Perineum  and  back  of  scro- 

ral.           | 

>      turn.     Anus. 

DISEASES   OF  THE  NERVOUS   SYSTEM.  II 

peculiar  to  man  and  the  higher  apes.  Each  group  of  cells  pre- 
sides over  the  action  of  a  muscle  and  maintains  its  tone  and 
nutrition,  so  that  all  motor  impulses  to  the  muscle,  whether  reflex, 
automatic,  or  voluntary,  proceed  from  the  group  of  cells.  The 
outer  groups  govern  muscles  of  flexion,  extension,  pronation  and 
supination  of  the  larger  joints.  The  inner  groups  govern  the 
small  muscles  of  the  fingers  and  toes.  Hence  the  outer  groups 
are  said  to  preside  over  fundamental  motions  and  the  inner 
groups  over  accessory  motions. 

The  thumbless  monkey  has  no  inner  groups  in  the  cervical 
region.  These  are  present  in  monkeys  with  thumbs  and  in  man. 
When  the  inner  groups  are  Destroyed  by  disease,  the  finger  mo- 
tions are  paralyzed. 

In  each  segment  there  may  be  from  two  to  eight  groups  of 
cells.  Any  group  may  extend  through  several  segments.  If  a 
single  segment  is  destroyed  by  disease  several  muscles  will  be 
paralyzed.  But  no  muscle  will  be  totally  paralyzed  unless  its 
entire  group  of  cells  is  destroyed.  Total  paralysis  with  complete 
atrophy  in  a  muscle  indicates  destruction  of  the  entire  group  of 
cells  which  govern  the  muscle.  If  the  group  extends  through 
several  segments  the  paralysis  implies  disease  in  all  the  seg- 
ments. The  table  shows  the  situation  in  the  various  segments 
of  the  groups  of  cells  governing  the  various  muscles,  so  far  as 
these  have  been  determined. 

ANTERIOR  POLIOMYELITIS. 

Anterior  Poliomyelitis  is  a  disease  limited  to  the  anterior  horns 
of  the  spinal  cord.  It  may  be  acute  or  chronic. 

Acute  anterior  poliomyelitis  is  a  common  disease  of  childhood 
known  as  infantile  paralysis.  It  occasionally  occurs  in  adults. 
Chronic  anterior  poliomyelitis  is  an  uncommon  disease  of  adult 
life  or  old  age,  known  as  atrophic  paralysis. 

Acute  Anterior  Poliomyelitis.  Etiology. — Occurs  chiefly  between 
two  to  five  years,  when  exertion  is  greatest,  in  the  summer, 
May  to  September,  when  exposure  is  greatest  to  heat,  occasion- 
ally after  falls  and  after  fevers  ;  it  is  probably  an  acute  infectious 
disease  in  many  cases. 

Pathology. — Lesion  is  an  acute  inflammation  of  the  entire  gray 
matter  of  the  anterior  horn,  the  cells  and  interlacing  fibres  being 
affected.  The  cells  become  swollen,  undergo  degeneration,  and 
liquefy,  and  then  shrivel  and  atrophy.  The  fibres  are  separated 


12  DISEASES   OF   THE   NERVOUS   SYSTEM. 

from  their  cells  and  atrophy.  The  neuroglia  is  infiltrated  with 
inflammatory  corpuscles.  The  capillaries  are  distended  and  fre- 
quently rupture.  The  process  may  go  on  to  complete  destruc- 
tion of  the  cells  or  may  be  arrested  at  any  stage. 

If  it  is  arrested  early,  repair  may  ensue  and  the  cells  regain 
their  former  appearance.  If  it  goes  on  the  result  is  a  diminution 
in  the  size  of  the  horn,  a  change  in  its  shape  and  a  contraction 
of  the  entire  cord  at  the  level  of  the  lesion. 

As  a  rule  the  entire  anterior  horn  is  at  first  involved,  but  the 
permanent  destruction  is  limited  to  one  or  two  groups  of  cells 
on  one  side  only. 

In  as  much  as  each  motor  nerve^bre  comes  from  and  is  a  part 
of  the  motor  cell  the  nerve  fibres  degenerate  when  the  motor  cells 
are  destroyed.  Atrophy  of  the  motor  nerve-roots  and  motor- 
nerves  from  the  anterior  horns  to  the  muscles  is  therefore  part 
of  the  lesion  in  anterior  poliomyelitis.  The  deformity  of  the 
spinal  cord  at  the  level  of  the  lesion,  and  the  atrophy  of  the  nerve 
trunks  are  due  in  part  to  these  changes  in  the  nerve  fibres. 

The  muscles  which  are  paralyzed  atrophy  rapidly,  and  when 
recovery  does  not  occur  they  remain  small. 

Mije  no   special  groups  of  cells  are   known  to  control  the 
3 


3n-of  the  bones,  it  is  found  that  if  the  gray  matter  near 
the  central  region  of  the  segment  is  destroyed  by  the  diseas,e,  the 
bones  are  much  retarded  in  their  growth.  Hence  in  a  severe 
case  of  infantile  palsy  the  limb  affected  is  smaller  than  other 
limbs  in  all  its  parts.  But  trophic  changes  in  the  skin,  such  as 
sores,  glossy  skin,  or  gangrene,  do  not  occur.  Through  the  an- 
terior horns  pass  fibres  from  the  central  region  which  control  the 
vascular  tone  and  metabolic  processes.  Hence  in  lesions  of  the 
anterior  horn  symptoms  due  to  the  destruction  of  these  fibres 
ensue,  viz.,  sluggish  circulation,  cyanosis,  and  lowered  tem- 
perature, with  imperfect  nutrition. 

Symptoms.  —  Sudden  onset  with  fever  100°  to  103°  F.,  occa- 
sionally without.  Febrile  symptoms  :  Headache,  loss  of  appetite, 
nausea,  vomiting,  diarrhoea.  Restlessness  :  often  convulsions 
and  delirium.  The  fever  rarely  continues  more  than  two  tp  three 
days.  Occasionally  pain  in  the  back  and  limbs  is  complained  of 
when  child  is  old  enough  to  talk. 

Paralysis  appears  suddenly.  Sometimes  is  found  in  the*  morn- 
ing ;  is  complete  and  extensive  either  in  one  limb  or  more  ;  legs 
oftener  than  arms,  4  to  i  ;  one  limb  more  than  the  other.  Maxi- 


DISEASES   OF  THE   NERVOUS   SYSTEM.  13 

mum  is  reached  in  first  week.  Remains  stationary  for  two  to  six 
weeks  and  then  improves.  Result  is  recovery,  which  is  partial ; 
some  muscles  remain  paralyzed.  The  affected  limb  atrophies 
rapidlv.  Atrophy  is  most  intense  in  the  muscles  permanently 
weak.  There  is  a  change  in  the  electric  reactions  in  the  paralyzed 
muscle.  R.  D.  Loss  of  faradic  excitement  in  two  weeks  or  sooner. 
Increase  at  first,  then  decrease,  in  galvanic  excitability.  Muscles 
contract  slowly  instead  of  quickly,  more  forcibly  to  the  positive 
than  to  the  negative  pole. 

The  nutrition  of  the  entire  limb  suffers  ;  bones  small  and 
growth  impaired  ;  fat  is  less  frrm,  ano>  skin  is  cold  ;  but  no  bed- 
sores appear.  The  sphincters  are  not  affected.  The  reflex  action 
is  lost  at  the  level  affected,  not  changed  elsewhere. 

Course. — There  is  a  progressive  improvement  which  begins 
within  two  months,  but  usually  some  muscles  remain  paralyzed 
and  atrophied,  and  the  joints  moved  by  these  may  become  de- 
formed ;  spine  curved.  The  muscles  most  frequently  affected  are  : 
The  peronei  and  tibialis  anticus  in  the  leg,  hence  talipes  equinus 
and  varus  ;  the  muscles  of  the  calf,  and  anterior  part  of  the  thigh  ; 
the  deltoid,  biceps,  supinators,  and  spinati  in  the  arm,  hence 
subluxation  of  humerus ;  the  muscles  of  the  hand  and  fore- 
arm. 

General  health  is  unaffected.  / 

In  adults  acute  anterior  poliomyelitis  presents  the  same  symp- 
toms, but  fever  is  less  severe  and  pain  is  greater  in  muscles. 
Extent  of  initial  paralysis  is  greater.  ^Occasionally  the  onset  is 
slow  so  that  case  is  called  subacute,  developing  in  two  to  four 
weeks  progressively,  remaining  10r«^ri;ime  stationary  and  then 
subsiding?* 

Diagnosis. — From  acute  rheumatism  in  infants.  Rheumatism 
may  produce  immobility  of  joints.  It  also  causes  pain,  redness, 
swelling  of  joints,  and  tenderness. 

Prognosis. — Good  as  to  life. 

As  to  recovery,  at  end  iff  two  weeks  test  faradic  reaction.  The 
muscles  in' which  it  persists  will  recover  entirely. 

At  end  of  three  months  test  again.  The  muscles  in  which  it  has 
returned  wilj  recover  partially. 

At  end  of  six  months  test  again.  The  muscles  which  do  not  re- 
spond will  never  recover. 

As  to  use  of  lin>b  it  depends  on  growth  of  bone ;  e.g.,  short  leg 
on  developn^nt  of  deformity  and  'contractures  ;  e.g.,  talipes. 


-. 


14  DISEASES   OF   THE   NERVOUS   SYSTEM. 

Treatment. — In  acute  stage  :  Cup  or  blister  the  spine  and  keep 
quiet.  Give  ergot  and  bromide,  and  antipyretics. 

In  chronic  stage  :  Rubbing,  warm  clothing,  galvanism  to  the 
muscles,  interrupted,  continuous.  Strychnine  T^  to  -^  t.i.d.,  ac- 
cording to  age.  Prevent  or  remedy  deformities  by  apparatus  or 
surgical  operation. 

Chronic  Anterior  Poliomyelitis. — Progressive  muscular  atrophy 
occurs  in  adults  between  thirty  and  fifty  years  ;  is  a  rare  disease. 

Etiology. — Falls  and  injuries,  exposure  to  damp  and  cold,  alco- 
holic and  sexual  excesses,  lead  poison  ing  (?). 

Symptoms. — Gradually  increasing  atrophic  paralysis,  several 
months  in  onset,  preceded  by  fatigue  and  weakness  and  loss  of 
weight.  Muscles  become  flabby,  then  atrophied  and  paralyzed. 

It  begins  in  legs  and  extends  upward  (peroneal  type). 

It  may  begin  in  hands  and  then  extend  to  shoulders  and  in- 
vade the  back  (Aran  Duchenne  type). 

Finally,  all  the  muscles  of  the  body,  including  face  and  tongue, 
may  be  affected.  The  tendon  reflexes  are  lost. 

There  are  fibrillary  twitchings  in  muscles. 

There  are  electrical  changes  which  vary  in  different  cases, 
usually  R.  D.  is  found. 

The  circulation  is  poor  in  the  limb,  skin  cold  and  blue. 

There  is  no  sensory  disturbance  except  slight  numbness. 

There  are  no  visceral  symptoms,  no  disturbance  of  bladder 
and  rectal  control.  Bedsores  do  not  develop. 

Course. — Gradual  increase  after  a  long  period  of  stationary 
state.  Sometimes  a  steady  progress  to  bulbar  paralysis  and 
death. 

Treatment. — Similar  to  chronic  stage  of  acute  anterior  polio- 
myelitis. 

CRANIAL  NERVE  NUCLEI. 

The  groups  of  cells  in  the  cerebral  axis  (medulla  oblongata, 
pons  varolii,"  and  crura  cerebri)  which  give  origin  to  the  motor 
cranial  nerves  lie  partly  on  the  floor  of  the  fourth  ventricle  (XII., 
VI.,  IV.,  III.),  and  partly  deep  beneath  the  floor  in  the  formatio 
reticularis  (XL,  IX.,  VII.,  Vm.).  These  groups  of  cells  are  quite 
homologous  to  the  groups  in  the  anterior  horns  of  the  cord,  and 
are  subject  to  diseases  whose  pathology  is  the  same  of  that  of 
poliomyelitis. 


DISEASES   OF  THE   NERVOUS   SYSTEM.  1 5 


BULBAR  PARALYSIS— OR  GLOSSO-LABIO-LARYNGEAL  PARALYSIS 

(Rare). 

Symptoms. — Slowly  progressing  paralysis  with  atrophy  in  the 
motor  cranial  nerve  nuclei  muscles. 

1.  Disturbance  of  speech.     Alalia,  tongue  letters,  R  L  D  T, 
due  to  paralysis  of  XII.  nerve  nucleus.     Atrophy  and  tremor  of 
tongue  with  paralysis.     Chewing,  swallowing  impaired. 

2.  Muscles  of   lips   and  face  become  weak  and  thin,  due  to 
paralysis  of  VII.  nerve  nucleus.     Alalia  extends  to  lip  letters,  P 
B  V  F.     Atrophy  and  tremor  of  lips  with   paralysis.     Whistling, 
facial  expression  impaired.      Saliva  runs  and  is  increased. 

3.  Muscles  of  pharynx  and  larynx  affected,  due  to  paralysis 
of  the  IX.  and  XI.  nerve  nuclei.    Food  regurgitates  or  cannot  be 
swallowed  ;  reflex  action  impaired  ;  larynx   unprotected  ;    voice 
monotonous,  low  ;  cough  impossible. 

There  is  no  change  of  sensation  or  of  taste. 

Pulse  sometimes  rapid,  100  to  130. 

Duration  two  to  five  years. 

Death  from  inanition,  pneumonia,  heart  failure. 

OPHTHALMOPLEGIA. 

This  is  a  rare  disease  due  to  an  atrophy  of  the  nuclei  of  the 
nerves  moving  the  eyeball. 

The  muscular  apparatus  of  the  eye  consists  of  external  mus- 
cles moving  the  eyeball :  Recti  and  obliqui  and  levator  palpe- 
brae.  Internal  muscles  moving  the  iris :  Dilators  and  constrict- 
ors. Each  of  these  may  be  affected  alone  or  together. 

(  externa. 
Ophthalmoplegia  jinterna 

Ophthalmoplegia  Externa.  Symptoms. — Gradually  increasing  loss 
of  power  in  all  the  muscles  of  eyeball.  One  or  more  muscles  at 
first,  then  others,  till  all  are  affected. 

Result,  ptosis.  Various  forms  of  strabismus,  nystagmus,  and 
finally  immobility  of  eyeball.  Double  vision. 

Ophthalmoplegia  Interna.  Symptoms. — Loss  of  reflex  to  light. 
Occurs  as  a  symptom  in  locomotor  ataxia  and  general  paresis. 

Diagnosis. — From  paralysis  of  single  nerves,  III.  nerve  or 
VI.  nerve,  by  the  fact  that  such  disease  is  unilateral  and  all  the 


l6  DISEASES   OF  THE   NERVOUS   SYSTEM. 

muscles  supplied  by  the  single  nerve  are  involved,  others  remain- 
ing unaffected,  and  by  the  fact  that  the  pupil  is  always  affected. 

PROGRESSIVE  MUSCULAR  DYSTROPHY. 

This  is  a  primary  muscular  disease  which  results  in  atrophy 
and  paralysis.  It  is  commonly  mistaken  for  chronic  anterior 
poliomyelitis  or  progressive  muscular  atrophy,  but  differs  from 
this  in  causation,  symptoms,  and  pathology. 

Causation. — It  is  an  hereditary  affection,  or  a  disease  of  devel- 
opment or  of  nutrition.  It  develops  in  several  children  in  same 
family  with  same  or  various  types. 

Pathology. — The  lesion  is  an  essential  and  primary  change  in 
the  muscle  fibres. 

1.  Individual  fibres  become  hypertrophied. 

The  nuclei  of  the  muscle  fibres  are  increased  in  number. 

Then  vacuoles  appear  as  evidence  of  degeneration  and  fibres 
split  up. 

At  the  same  time  there  is  an  increase  in  connective  tissue 
about  the  muscle  fibres. 

Sometimes  there  is  a  development  of  fat  between  the  muscle 
fibres. 

2.  Subsequently  to  the  hypertrophy  and  sometimes  without 
it  atrophy  of  the  muscle  fibres  occurs  with  same  development 
of  fat  and  connective  tissue  or  without  it. 

Appearance  during  hypertrophy  is  a  very  fat  limb  in  which 
muscles  are  really  weak  ;  during  atrophy  is  a  very  thin  limb  in 
which  muscles  are  very  weak  or  even  totally  paralyzed. 

Symptoms. — In  all  forms  there  develops  a  progressive  simulta- 
neous weakness  and  atrophy  of  the  muscles  affected  going  on 
slowly  to  complete  paralysis.  The  consequences  of  such  paraly- 
sis are  evident  in  size,  posture,  and  deformities,  use,  motion,  and 
gait. 

No  fibrillary  twitching  vs.  progressive  muscular  atrophy. 

No  R.  D.  vs.  chronic  anterior  poliomyelitis. 

No  sensory  disturbance,  bladder,  or  rectal,  or  trophic  skin 
changes. 

Various  types  of  the  disease  classified  by  Erb  : 

I.   Infantile  muscular  dystrophy. 

i.   Hypertrophic  in  type. 

Pseudo-hypertrophy — fat  only. 
True  hypertrophy,  muscle  also. 


DISEASES   OF   THE    NERVOUS   SYSTEM.  17 

2,  Atrophic  type. 

In  limbs  only. 

In  limbs  and  face  also. 
II.  Adult  muscular  dystrophy,  with  similar  classes. 

1.  INFANTILE  MUSCULAR   DYSTROPHY. — HYPERTROPHIC  FORM. 

i.  Pseudo-hypertrophic  Paralysis. — Children  aged  from  two  to 
eight  affected,  males  more  than  females.  Only  twenty-five  per 
cent,  occur  after  twenty  years.  Several  in  one  family. 

Begins  with  difficulty  in  gait.  Cannot  walk,  go  up-stairs,  or 
get  up. 

Muscles  of  back  atrophied,  and  calves  of  legs  hypertrophied. 
Also  infraspinatus  and  deltoid  hypertrophied. 

Other  muscles  atrophy,  pectorales,  latissimus  dorsi,  triceps, 
and  muscles  of  thighs. 

Posture,  shoulders  far  back.  Gait  is  waddling  and  mode  of 
rising  by  climbing  up  the  legs  due  to  paralysis  of  extensors  of 
hip  is  characteristic. 

Finally  inability  to  sit  up  from  paralysis  of  trunk. 

After  paralysis  has  occurred  shortening  of  muscles  follows 
and  deformities,  talipes  equinus  and  curvature  of  spine. 

No  R.  D.  Knee-jerk  normal,  then  weak.  Sensation  and 
sphincters  not  involved. 

Death  is  due  to  some  intercurrent  malady,  occurs  between 
twelve  and  twenty  years  of  age. 

Only  treatment  is  exercise. 

2.  True  Hypertrophic  Paralysis   (juvenile   muscular  atrophy). 
Develops  in  children  six  to  ten.     Several  in  a  family.     Begins 
with  progressive  weakness  of  muscles. 

Muscles  affected  with  hypertrophy  are,  deltoid,  infraspinatus, 
muscles  of  forearm,  sartorius,  gastrocnemii. 

Muscles  which  atrophy  are,  pectorales,  latissimus  dorsi,  ser- 
ratus  magnus,  biceps,  coracobrachialis,  supinator  longus,  adduc- 
tors of  thighs,  glutei  and  back  muscles  ;  finally  calf  and  peronei. 

Gait,  posture  and  deformities  are  characteristic.  No  fib- 
rillary  contraction.  No  R.  D.  Knee-jerk  slowly  diminished.  No 
disturbance  of  sensation  or  of  sphincters. 

3.  Atrophic    Type  in   Body   and  Limbs    (hereditary    muscular 
atrophy).     Same  features,  except  entire  absence  of  hypertrophy. 
Develops  from  eight  to  ten  years. 


18  DISEASES   OF   THE   NERVOUS   SYSTEM. 

4.  Atrophic  Type  in  Limbs  and  Face  (infantile  muscular  atro- 
phy ;  Landouzy  Dejerine  type).  Face  is  often  first  affected. 

When  face  is  involved  the  zygomatic  muscles  are  affected 
first ;  loss  of  naso-labial  fold  ;  flat  mask-like  face  ;  lower  lip  pro- 
jects ;  orbicularis  is  affected  ;  lips  open  ;  labials  can't  be  spoken. 
Sometimes  orbic.  palpebrae  weak.  Facial  muscles  atrophy  slowly. 

The  other  muscles  of  the  body  are  affected  in  succession 
much  later,  pectorals,  latissimus  dorsi,  biceps  and  triceps.  Del- 
toids may  be  hypertrophied.  Back  muscles  and  extensors  of 
thighs  are  invaded. 

Gait,  posture,  same  as  in  other  types. 

II.  ADULT  MUSCULAR  DYSTROPHY. 

Any  of  these  forms  may  occur  in  adults.  Usually  a  family 
history  can  be  obtained.  Usually  develops  about  age  of  eigh- 
teen, sometimes  not  till  thirty.  Some  muscles  are  hypertrophied 
others  atrophied  as  in  infantile  types. 

THE    CENTRAL  GRAY    MATTER   OF   THE    SPINAL    CORD   AND   ITS 

DISEASES. 

The  portion  of  gray  matter  lying  behind  the  anterior  horn, 
and  adjacent  to  the  central  canal  of  the  spinal  cord  and  extend- 
ing backward  to  the  posterior  horn,  is  made  up  of  gelatinous  gray 
substance  and  of  scattered  nerve-cells  with  a  plexus  of  fibres.  It 
contains  one  long  column  of  flask-shaped  cells — the  column  of 
Clarke — in  its  posterior  median  part ;  and  an  irregular  column  of 
small  cells  in  its  lateral  part  —  the  intermedio-lateral  column. 
The  majority  of  these  cells  differ  from  the  cells  of  the  anterior 
horn,  in  not  having  a  long  axis  cylinder  process  which  enters  a 
nerve.  They  have  numerous  branching  processes,  some  send- 
ing a  long  branch  to  the  other  side  through  the  anterior  com- 
missure, others  sending  a  branch  out  into  the  antero-lateral 
column  where  it  bifurcates,  turning  up  and  down,  and  in  its 
course  gives  off  collaterals,  which  enter  the  gray  matter  at  vari- 
ous levels.  These  cells  thus  form  an  associated  system  within 
the  cord. 

The  function  of  the  central  gray  matter  is  to  preside  over,  i, 
vasomotor  tone  ;  2,  nutrition  of  all  parts  ;  3,  visceral  activity,  in- 
cluding digestion  and  excretion,  and  the  activities  regulated  by 
the  sympathetic  system. 


DISEASES   OF   THE   NERVOUS   SYSTEM.  1 9 

i  i.  Vaso-motor  innervation  is  a  reflex  matter  requiring  centres 
with  sensory  and  motor  nerves.  Gaskell  has  proven  that  these 
lie  in  the  central  gray  matter  and  are  joined  by  fine  nerve-fibres 
which  pass  in  the  nerve-roots  through  the  two  horns  of  the  cord. 
The  regulation  of  the  flow  of  blood  in  accordance  with  the  need 
of  an  organ  is  governed  here. 

2.  The  proper  degree  of  metabolism  necessary  for  nutrition  in 
the  skin,  bones,  and  joints  and  muscles,  or  for  repair  of  tissue,  is 
under  the  control  of  nerves  whose  centres  are  in  the  central  gray 
matter. 

3.  The  sympathetic  system  of  nerves  presides  directly  over  di- 
gestion, circulation,  secretion,  and  excretion,  but  is  in  turn  con- 
trolled by  spinal  centres  which   lie   in  the  entire  length  of  the 
spinal  cord  in  the  central  gray   matter.     See  Gowers,  I.,  pp.  205 
to  209. 

The  central  gray  matter  receives  sensory  impulses  of  pain  and 
temperature  sense  and  transmits  these  for  some  distance  on  their 
way  upward  after  they  reach  it  through  the  posterior  nerve- 
roots  ;  each  segment  of  the  cord  being  related  to  its  own  part  of 
the  surface  as  shown  in  the  table. 

All  these  functions  are  disturbed  in  diseases  of  the  central 
gray  matter. 

SYRINGO-MYELITIS. 

Pathology. — This  is  a  rare  disease,  of  congenital  origin,  charac- 
terized by  a  development  of  gliomatous  tissue  in  the  gray  matter 
around  the  central  canal,  which  subsequently  extends  outward 
involving  the  entire  central  gray  matter,  and  then  degenerates 
and  liquefies,  leaving  a  cavity  in  the  spinal  cord.  Such  a  cavity 
may  extend  through  a  part  of  the  cord,  or  through  its  entire 
length  ;  varying  in  size  at  different  segments  and  thus  destroy- 
ing more  or  less  of  the  gray  matter.  Its  usual  situation  is  in 
the  lower  cervical  and  upper  dorsal  regions.  The  disease  may 
invade  the  anterior  horns  of  the  cord,  causing  the  symptoms  of 
chronic  anterior  poliomyelitis.  It  may  invade  the  posterior 
horns  and  columns,  causing  symptoms  of  posterior  sclerosis. 

Symptoms. — i.  Loss  of  the  sensations  of  temperature  and  pain 
while  the  sensations  of  touch  and  location  are  retained.  The  dis- 
tribution of  this  sensory  disturbance  depends  on  the  location  of 
the  disease,  e.g.,  if  the  left  hand  and  forearm  only  are  thus 
affected  the  disease  must  be  limited  to  the  left  side  of  the  cervi- 


20  DISEASES   OF  THE   NERVOUS   SYSTEM. 

cal  region  of  the  cord  in  its  lower  third,  which  receives  sensations 
from  these  parts.     Such  disturbance  of   sensation  may  be  exten- 
sive, involving  irregular  areas  of  the  body.     It  is  never  symmet-^ 
rical  on  both  sides. 

2.  Vasomotor   and    trophic    symptoms.      Cyanosis,    oedema, 
blueness  of  extremities,  with  lowering  of  temperature,  ulcers,  bul- 
lous   eruptions,    sweating,    thickened    or   glossy   skin,  defective 
growth  of  the  nails,  great  brittleness  of  the  bones  leading  to  re- 
peated fractures,  and  joint  affections,  also  progressive  atrophy  of 
the  muscles.     These  occur  usually  in  one  limb  only. 

3.  Disturbance   in    and    loss   of   control   over   the  action  of 
bladder  and  rectum,  and  loss  of  sexual  power  are  present  when 
the  lumbar  region  of  the  spinal  cord  is  invaded. 

4.  Paralysis  of  the   spinal   muscles   with    curvatures    of  the 
spine. 

Course  of  the  disease  is  chronic,  with  slow  progress  till  the 
symptoms  are  developed,  often  including  the  symptoms  of  chronic 
anterior  poliomyelitis.  It  then  remains  stationary,  but  if  it  ad- 
vances upward  and  invades  the  medulla,  death  may  occur  at  any 
time  from  paralysis  of  the  heart  and  respiration. 

The  prognosis  is  bad  and  no  treatment  can  stop  the  course. 

When  tumors  destroy  the  central  gray  matter  or  hemorrhages 
occur  in  it,  the  same  terminal  symptoms  may  be  expected  as  in 
syringo-myelitis. 

THE  POSTERIOR  HORNS  OF  THE  CORD. 

This  portion  of  the  cord  is  made  up  partly  of  gelatinous  mat- 
ter which  occupies  its  extremity,  and  partly  of  a  fine  plexus  of 
nerve-fibres,  in  which  small  cells  are  irregularly  scattered.  The 
function  of  the  posterior  horn  is  to  receive  the  impulses  coming 
in  through  the  posterior  nerve-roots,  and  to  transmit  such  im- 
pulses in  various  directions.  These  are  the  sensations  of  touch, 
temperature,  pain,  pressure,  and  location,  and  of  the  muscular 
sense. 

Each  nerve  of  sensation  gives  off  numerous  branches  on  en- 
tering the  cord,  and  finally  terminates  in  a  brush-like  expansion 
of  nerve  fibrils  which  surrounds  some  nerve-cell,  or  in  the  plexus 
of  nerve-fibrils  which  make  up  a  fine  felt-like  tissue  in  the  pos- 
terior horn.  Any  fibre  after  entering  the  posterior  nerve-root 
may  pass  directly  into  the  posterior  horn,  or  may  turn  up  or 
down  in  the  white  matter  near  the  horn  and  enter  the  posterior 


DISEASES   OF   THE   NERVOUS   SYSTEM.  21 

horn  at  some  level  other  than  that  of  its  entrance.  The  posterior 
horns  are  continuous  upward  (through  the  medulla  and  pons) 
with  the  ascending  root  of  the  fifth  nerve.  The  diseases  of  the 
posterior  horn  will  be  considered  with  diseases  of  the  posterior 
roots  and  columns,  as  they  uniformly  coincide. 

THE   WHITE    COLUMNS    OF    THE    SPINAL    CORD    AND    THEIR    DIS- 
EASES. 

The  gray  matter  of  the  spinal  cord  is  surrounded  by  white 
tissue  made  up  of  anterior  and  posterior  nerve-roots  and  of  nerve- 
fibres  passing  up  or  down  the  cord  for  longer  or  shorter  dis- 
tances. The  white  columns  contain  therefore  : 

1.  Fibres  joining  the  skin,  joints,  muscles,  and  viscera  to  the 
gray  matter  of  the  spinal  cord  and  entering  the  various  segments 
through  the  anterior  and  posterior  nerve-roots. 

2.  Fibres  connecting  the  various  segments  with  one  another. 

3.  Fibres  joining  the  various  segments  with  the  brain. 

The  white  matter  can  be  divided  into  different  columns  by 
observing  the  process  of  development — different  columns  develop 
at  different  periods  of  foetal  life  ;  or  by  studying  the  process  of 
disease — different  diseases  select  different  columns. 

These  columns  and  their  diseases  are  as  follows  : 

THE  MOTOR  COLUMNS. 

1.  Anterior  median  column. 

2.  Lateral  pyramidal  column. 

At  the  lower  limit  of  the  medulla  each  anterior  pyramid  di- 
vides into  two  parts;  one  part  passes  directly  on  into  the  an- 
terior median  column  of  the  cord  ;  the  other  part  crosses  over  to 
the  opposite  lateral  column  of  the  cord,  lying  near  to  the  gray 
matter  in  the  angle  between  the  anterior  and  posterior  horn. 
As  the  fibres  making  up  these  columns  pass  down  the  cord  they 
turn  into  the  anterior  gray  horns  of  the  different  segments — 
each  column  becoming  smaller  the  lower  it  goes.  The  anterior 
median  column  is  exhausted  at  the  lower  dorsal  cord  and,  there- 
fore, does  not  exist  in  the  lumbar  region.  The  lateral  pyramidal 
column  extends  to  the  lowest  segment  of  the  cord.  These  col- 
umns transmit  motor  impulses  from  the  motor  cortex  of  the 
brain  and  from  the  motor  ganglia  of  the  brain  to  the  spinal  motor 
centres.  These  columns  also  contain  fibres  whose  origin  is  in 


22  DISEASES   OF  THE   NERVOUS   SYSTEM. 

the  pons  and  cerebellum,  which  pass  with  the  motor  fibres  from 
the  brain  and  terminate  in  the  anterior  horns  of  the  cord. 

They  also  contain  fibres  of  association  passing  between  vari- 
ous segments  of  the  cord.  All  these  sets  of  fibres  degenerate 
downward.  The  area  of  degeneration  is  less  in  extent  when  the 
lesion  is  in  the  brain  than  when  it  is  in  the  cord  itself. 

LATERAL  SCLEROSIS. 

Lateral  sclerosis  is  a  chronic  sclerotic  process  affecting  the 
lateral  pyramidal  columns  of  the  spinal  cord. 

It  may  be  primary  and  is  then  bilateral. 

It  may  be  secondary  to  other  diseases  in  the  brain  or  cord 
which  separate  the  fibres  of  the  motor  tract  from  their  centres 
of  origin  and  nutrition  in  the  brain  cortex.  Such  diseases  are  : 

1.  Tumors,  softening  or  hemorrhage  in  the  brain,  destroying 
the  motor  tract  in  one  hemisphere,  in  which  case  the  secondary 
sclerosis  is  found  in  the  anterior  median  column  and  the  oppos- 
ite lateral  pyramidal  tract. 

2.  Congenital   maldevelopment  of  the  brain   and  hydroceph- 
alus,  affecting  both  motor  tracts,  in  which  case  both  anterior  me- 
dian and  both  lateral  columns  are  sclerotic. 

3.  Any  lesion  in  the  spinal  cord,  either  unilateral  or  bilateral, 
or  compression  of  the  cord  by  disease  of  the  vertebrae,  in  which 
case  the  sclerosis  only  appears  below  the  level  of  the  lesion,  and 
its  extent  is  greater  in  area  than  in  i  or  2. 

Pathology  of  Sclerosis. — i.  An  increase  in  the  thickness  of  the 
connective-tissue  framework  which  supports  the  nerve-fibres. 
2.  A  primary  degeneration  or  a  secondary  destruction  of  the 
axis  cylinder  in  each  nerve-fibre,  resulting  in  its  swelling,  seg- 
mentation, fatty  degeneration,  and  final  absorption.  The  result 
is  to  reduce  the  number  of  fibres  in  any  column  of  the  cord,  or 
even  to  destroy  them  entirely,  the  place  of  the  fibres  being  filled 
by  connective  tissue. 

Symptoms  of  Primary  Lateral  Sclerosis,  or  Spastic  Paraplegia. — 
A  weakness  and  stiffness  in  motion,  beginning  in  the  legs  and 
ascending,  finally  involving  the  arms.  The  muscles  affected  do 
not  atrophy  rapidly,  as  their  spinal  centres  are  not  diseased. 
Their  reflex  and  mechanical  excitability  is  increased,  as  the 
spinal  centres  are  no  longer  inhibited  by  brain  impulses.  Hence 
increased  knee-jerk  and  ankle  clonus  are  present.  They  be- 
come rigid  from  the  increased  spinal  activity.  Hence  the  gait 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


is  at  first  "spastic"  (toes  drag,  knees  overlap,  motion  stiff), 
finally,  when  paralysis  is  complete,  the  legs  are  drawn  up,  knees 
overlapping  and  so  rigid  as  to  be  incapable  of  passive  motion. 
There  are  no  electric  changes  in  the  muscles. 

The  action  of  the  bladder  is  imperfectly  controlled,  and  finally 
involuntary  emptying  of  the  bladder  at  intervals  or  retention  of 
urine  occurs.  Constipation  is  obstinate.  In  some  cases  of  pri- 
mary lateral  sclerosis  the  bladder  and  rectum  are  not  affected. 
The  vascular  tone  is  decreased  toward  the  close  of  the  disease 
and  nutrition  is  impaired.  There  are  no  sensory  symptoms. 

Course  of  the  Disease. — The  symptoms  develop  slowly  and  in- 
crease until,  after  many  years,  permanent  paralysis  has  de- 
veloped. 

Secondary  Lateral  Sclerosis  presents  the  same  symptoms  on  one 
or  both  sides,  but  the  symptoms  develop  more  rapidly  according 
to  the  nature  of  the  primary  disease. 

Diagnosis  between  lateral  sclerosis  and  anterior  poliomyelitis  : 


Lesion  in  pyramidal  tracts. 

Paralysis  usually  on  both  sides  equally, 
in  legs,  or  in  legs  and  arms,  never  in 
arms  alone. 

All  muscles  are  about  equally  affected.  No 
muscles  are  entirely  normal. 

Muscular  tone  is  heightened. 

Tendency  to  rigidity  appears. 

Reflex  excitability  is  increased. 

A  trofliy  is  absent,  or  is  slight ;  and  merely 
due  to  disuse,  hence  is  gradual  in  prog- 
ress. It  affects  the  entire  limb. 

Electric  contractility  is  unchanged. 


Vascular  tone   is  diminished ;    cyanosis 

and  oedema  may  occur. 
Paralyzed  limb  is  cold,  and  sweat  may  be 

increased. 
Trophic  disturbances  in  the  skin  are  not 

infrequent. 
The  control  over  the  bladder  and  rectum 

may  be  diminished  or  lost. 


Lesion  in  anterior  gray  horns. 

Paralysis  may  be  limited  to  any  single 
limb,  and  rarely  affects  both  limbs 
equally. 

Certain  groups  of  muscles  only  are  af- 
fected. Others  escape  wholly. 

Muscular  tone  is  diminished. 

Muscles  are  relaxed. 

Reflex  excitability  is  lost. 

Atrophy  is  always  present  in  the  paral- 
yzed muscles.  It  advances  rapidly, 
and  may  become  extreme. 

Electric  contractility  is  changed.  Reac- 
tion of  degeneration  is  present  within 
two  weeks  of  the  onset. 

Vascular  tone  is  diminished,  but  cedema 
does  not  occur. 

Paralyzed  limb  is  cool,  but  sweat  is  not 
increased. 

Trophic  disturbances  in  the  skin  do  not 
occur. 

The  control  over  the  bladder  and  rectum 
is  not  impaired. 


Treatment. — None.     [Read  Strumpell  on  spastic  spinal  paral- 
ysis and  on  compression  myelitis.] 


24  DISEASES   OF   THE   NERVOUS   SYSTEM. 


AMYOTROPHIC  LATERAL  SCLEROSIS. 

This  is  a  chronic  disease  affecting  the  entire  motor  system  of 
the  spinal  cord  and  cerebral  axis,  both  the  groups  of  cells  in  the 
anterior  horns  and  medulla  and  pons,  and  also  the  lateral  pyra- 
midal columns  in  the  cord  and  in  the  medulla  and  pons  being 
affected  together.  The  extent  of  the  sclerosis  is  greater  in  the 
cord  than  in  primary  lateral  sclerosis,  as  the  white  column  which 
lies  between  the  pyramidal  tract  and  the  gray  matter  (the  lateral 
limiting  column)  is  also  sclerotic  in  this  disease.  The  changes  in 
the  anterior  horns  are  the  same  as  in  chronic  anterior  polio- 
myelitis. 

Symptoms. — The  symptoms  present  features  similar  to  those 
of  chronic  anterior  poliomyelitis  and  of  extensive  secondary 
lateral  sclerosis.  Weakness,  paresis,  and  atrophy  begin  in  one 
or  both  arms  and  hands  and  increase  slowly.  The  muscles  of 
the  hands  and  the  extensors  of  the  wrist,  the  deltoid  and  triceps, 
are  the  muscles  chiefly  affected.  The  electric  contractility  is  di- 
minished, and  finally  reaction  of  degeneration  appears.  The 
muscular  irritability  and  reflexes  are  much  increased.  Finally 
contractures  result. 

Gradual  onset  of  spastic  paraplegia  in  the  legs  occurs  a  few 
months  after  the  arms  are  affected.  Spastic  gait  develops  with 
increased  reflexes.  In  the  final  stage  the  legs  are  totally  para- 
lyzed. There  are  no  sensory  disturbances,  and  bladder  and 
rectum  are  usually  under  good  control. 

After  several  years  symptoms  of  bulbar  paralysis  gradually 
develop,  with  paresis  and  atrophy  of  face,  tongue,  and  throat,  and 
death  occurs  from  respiratory  paralysis.  Occasionally  the  bulbar 
symptoms  appear  early. 

The  course  is  a  slow  one.  The  disease  may  be  arrested,  but 
recovery  is  impossible. 

Diagnosis  from  myelitis  of  the  cervical  region  and  from  syrin- 
go-myelitis  by  the  absence  of  sensory  symptoms  ;  from  anterior 
poliomyelitis  chronica  by  increased  mechanical  and  reflex  excit- 
ability in  muscles  atrophied,  and  by  development  of  spastic  gait. 

Treatment. — N  one. 


DISEASES   OF   THE   NERVOUS   SYSTEM.  25 


THE  SENSORY  COLUMNS. 

3.  Posterior  Lateral  Column,  or  Column  of  Burdach. 

4.  Posterior  Median  Column,  or  Column  of  Goll. 

5.  Marginal  Column,  or  Column  of  Lissauer. 

These  columns  are  made  up  chiefly  of  sensory  fibres  which 
enter  the  cord  in  the  posterior  nerve-roots.  They  also  contain 
fibres  of  association  between  different  segments  of  the  cord. 
Their  subdivisions  will  be  better  understood  by  a  study  of  the 
course  of  the  posterior  nerve-roots. 

The  posterior  nerve-roots  contain  two  sets  of  fibres.  The  ma- 
jority arise  from  the  cells  of  the  posterior  spinal  ganglia.  The 
minority  arise  from  the  so-called  tactile  corpuscles  of  the  ex- 
tremities. Each  spinal  ganglion  cell  has  two  branches,  or  two 
divisions  of  one  branch  ;  one  going  out  to  the  surface,  the  sen- 
sory nerve  ;  the  other  going  in  to  the  cord,  the  posterior  nerve- 
root.  The  cell  in  the  ganglion  nourishes  both  branches,  and  if 
either  branch  is  separated  from  its  cell  it  degenerates  in  its  entire 
length.  The  sensory  cranial  nerves  (X.,  IX.,  V.)  arise  from 
similar  ganglia  (jugtilare  Gasserian). 

The  posterior  nerve-root  enters  the  cord  opposite  to  the  apex 
of  the  posterior  horn  and  then  divides  into  two  bundles,  a  me- 
dian bundle  and  a  lateral  bundle. 

(i)  The  median  bundle  containing  large  fibres  enters  the  col- 
umn of  Burdach,  forming  its  root  zone  or  lateral  zone.  Here  a 
few  fibres  turn  downward  into  the  segment  next  below,  and  end 
in  the  posterior  horn  ;  but  the  large  majority  of  fibres  turn  up- 
ward to  go  to  higher  segments.  Some  of  these  soon  enter  the 
inner  side  of  the  posterior  horn  (short  fibres).  These  lie  near 
the  horn  in  the  lateral  zone.  Others  pass  up  through  several 
segments  (medium  fibres).  These  lie  nearer  to  the  median  line 
and  in  the  upper  cord  are  adjacent  to  the  column  of  Goll,  form- 
ing the  middle  zone  of  the  column  of  Burdach.  The  remainder 
pass  all  the  way  up  to  the  medulla  (long  fibres),  lying  at  first  in 
the  hinder  zone  of  the  column  of  Burdach  and  later  forming  the 
column  of  Goll.  For  as  each  root,  from  below  upward,  enters 
the  cord  it  displaces  inward  and  backward  the  fibres  already  as- 
cending ;  so  that  the  higher  the  level  the  larger  the  number  of 
ascending  fibres.  In  a  cross  section  of  the  cord  in  the  upper 
cervical  region  the  long  fibres  which  have  come  from  the  lumbo- 


26  DISEASES   OF  THE   NERVOUS   SYSTEM. 

sacral  region  occupy  the  column  of  Goll,  the  sacral  fibres  lying 
behind  the  lumbar  ;  the  long  fibres  from  the  dorsal  region  oc- 
cupy the  hinder  zone  of  the  column  of  Burdach  ;  the  long  fibres 
from  the  cervical  region  occupy  the  middle  zone  of  the  column 
of  Burdach.  It  is  evident  that  there  is  no  physiological  distinc- 
tion between  the  columns  of  Goll  and  Burdach.  In  the  anterior 
part  of  both  columns  near  the  gray  commissure  lie  association 
fibres  and  commissural  fibres.  It  is  thus  evident  that  the  median 
bundle  of  posterior  nerve-root  fibres  constitutes  the  columns  of 
Burdach  and  of  Goll. 

The  final  termination  of  these  fibres  is  as  follows  :  Each  fibre 
on  entering  the  cord  bifurcates,  a  short  branch  turns  down,  a 
long  branch  turns  up.  The  long  branch  in  its  course  upward 
gives  off  collateral  branches  which  pass  into  the  gray  matter  of 
the  posterior  horn,  and  finally  the  branch  itself  ends  there.  In 
all  cases  the  termination  is  by  means  of  a  brush-like  expansion 
of  nerve-fibrils.  The  short  fibres  end  in  the  fine  net-work  mak- 
ing up  the  substantia  gelatinosa  of  Rolando  in  the  posterior 
horn,  and  about  the  cells  of  the  posterior  and  central  gray  mat- 
ter. The  medium  fibres  end  in  a  net-work  which  surrounds  the 
cells  of  the  column  of  Clarke  in  the  central  gray  matter.  A  few 
fibres  pass  forward  to  the  anterior  horn  and  to  the  opposite  side 
through  the  posterior  gray  commissure.  The  long  fibres  pass 
up  to  the  nuclei  gracilis  and  cuneatus  in  the  medulla. 

(2)  The  lateral  bundle  of  the  posterior  nerve-root  consists  of 
both  large  and  small  nerve-fibres.  Many  of  these  pass  directly 
into  the  gray  matter  of  the  posterior  horn,  where  some  end  in  a 
net-work  of  fibres  about  the  cells  of  the  gelatinous  substance,  or 
deeper  in  the  horn  ;  and  others  pass  forward  and  cross  over  in 
the  gray  commissure  to  the  opposite  side,  where  they  turn  out- 
ward into  the  antero-lateral  column  or  backward  into  the  col- 
umn of  Goll.  The  smaller  fibres  bifurcate  on  entering  the  cord 
and  turn  down  and  up,  forming  the  column  of  Lissauer,  in 
which  they  pass  but  a  short  distance  and  then  turn  into  the  horn. 
This  column  is  of  uniform  size  through  the  cord  and  hence  can- 
not contain  any  long  fibres. 

6.  Antero-lateral  Ascending  Tract  or  Column  of  Gowers. — In  the 
antero-lateral  column  of  the  cord  lying  on  the  periphery  just  in 
front  of  the  direct  cerebellar  column  is  a  small  tract  which  as- 
cends through  the  cord  and  enters  the  formatio  reticularis  of 
the  medulla,  where  it  appears  to  end  in  the  gray  cells  of  this 


DISEASES   OF  THE   NERVOUS   SYSTEM.  27 

formation.  It  begins  in  the  lumbar  region,  and  increases  in  size 
as  it  ascends,  receiving  fibres  from  the  cells  of  the  central  gray 
matter.  It  degenerates  upward.  It  has  been  supposed  to  con- 
vey sensations  of  temperature  and  pain  upward  after  they  have 
passed  through  the  central  gray  matter. 

7.  Direct  Cerebellar  Column. — This  column  lies  on  the  lateral 
periphery  of  the  cord  just  outside  of  the  pyramidal  tract  and  be- 
hind the  antero-lateral  ascending  tract.  It  is  very  small  in  the 
upper  lumbar  region,  becomes  larger  in  the  dorsal  region,  and  is 
of  considerable  size  in  the  cervical  region.  Its  fibres  come  from 
the  cells  of  the  column  of  Clarke  in  the  central  gray  matter.  It 
passes  into  the  restiform  body  in  the  medulla  and  through  this 
into  the  cerebellum,  where  it  ends  in  the  vermiform  or  middle 
lobe.  It  is  supposed  to  convey  sensations  of  equilibrium  in  the 
act  of  walking. 

It  is  evident  that  the  sensory  fibres  from  the  posterior  nerve- 
roots  are  distributed  to  many  different  columns  of  the  spinal 
cord,  and  even  in  the  medulla  have  numerous  different  connec- 
tions. This  anatomical  fact  may  be  associated  with  the  physio- 
logical fact  that  one  sensation  is  capable  of  producing  several 
different  effects,  e.g.,  a  burn  causes  a  reflex  withdrawal  of  the 
part  burned,  vascular  changes,  and  a  process  of  repair,  sensa- 
tions of  heat,  touch,  and  pain,  accurately  localized,  followed  by 
conscious  effort  to  protect  the  part :  e.g.,  stumbling  in  the  act  of 
walking  causes  reflex  balancing  movements  involving  motions  of 
the  entire  trunk  and  arms  to  reestablish  the  centre  of  gravity  or 
protect  against  fall,  also  conscious  sensation  of  unstable  position, 
possibly  vertigo,  quickened  respiration,  action  of  ocular  muscles 
and  head  to  observe  danger,  sensation  of  contact,  possibly  pain, 
in  the  toes,  and  corresponding  vascular  changes  locally,  and 
finally  voluntary  effort  to  correct  position  after  an  appreciation 
of  all  the  various  sensations  received. 

We  distinguish  conscious  sensations  of  contact,  temperature, 
pain,  muscular  sense,  including  pressure  and  position,  and  un- 
conscious sensations,  which  set  up  reflex  and  automatic  acts, 
vascular  changes,  variation  in  thermic  and  nutritive  processes, 
and  changes  in  muscular  tone.  These  all  enter  by  the  posterior 
nerve- roots,  and  set  up  activities  in  the  central  nervous  system. 


28  DISEASES   OF  THE   NERVOUS   SYSTEM. 


LOCOMOTOR  ATAXIA. 

This  is  a  chronic  disease  of  the  sensory  part  of  the  nervous 
system,  the  posterior  nerve-roots  and  the  posterior  columns  of 
the  cord  being  diseased.  It  is  also  called  tabes  dorsalis,  or  posterior 
spinal  sclerosis. 

Pathology. — There  is  a  degenerative  neuritis  of  the  posterior 
nerve-roots,  and  sometimes  of  the  sensory  part  of  the  peripheral 
nerves.  There  is  a  sclerosis  of  the  posterior  columns  of  the 
spinal  cord,  beginning  in  the  lateral  or  root  zone  of  the  column 
of  Burdach  and  in  the  column  of  Lissauer,  extending  thence  to 
the  middle  zone  of  the  column  of  Burdach,  then  to  the  column 
of  Goll,  and  finally  to  the  hinder  zone  of  the  column  of  Burdach. 
Thus  both  posterior  columns  are  eventually  diseased  in  their 
entire  extent.  The  disease  usually  begins  in  the  lumbo-sacral 
region  and  extends  upward  through  the  cord.  It  is  many  years 
before  it  invades  the  cervical  region  or  destroys  the  entire  area 
of  the  posterior  columns.  The  terminal  net-work  of  nerve-fibres 
in  the  posterior  gray  matter,  and  especially  about  the  column  of 
Clarke,  is  destroyed  by  the  disease. 

Theories  of  the  disease:  (i)  It  is  a  primary  sclerosis  of  the 
posterior  columns  of  the  cord.  (2)  It  is  a  sclerosis  of  the  root- 
zone,  due  to  disease  of  the  vessels  entering  this  zone.  (3)  It  is  a 
primary  disease  of  the  cells  of  the  posterior  spinal  ganglia,  with 
secondary  degeneration  of  the  sensory  fibres  entering  the  cord 
from  the  ganglia,  and  compensatory  sclerosis  in  their  course. 

Etiology. — It  is  a  disease  of  adult  life,  persons  under  twenty- 
five  rarely  being  affected,  and  it  is  rare  among  women.  The 
chief  predisposing  cause  is  syphilis,  which  precedes  it  in  seventy 
per  cent,  of  the  cases.  The  exciting  causes  are  great  physical  exer- 
tion, exposure  to  cold  and  wet,  and  alcoholic  and  sexual  excesses. 

Symptoms. — The  symptoms  of  the  disease  are  very  numerous, 
but  appear  in  succession.  They  may  be  classified  according  to 
the  time  of  their  appearance.  There  is  a  stage  of  pain,  a  stage  of 
ataxia,  and  a  stage  of  paralysis. 

Symptoms  in  Stage  of  Pain. 

Paraesthesiae.  Numbness,  formication,  sensation  of  dead  ex- 
tremities, cotton  or  pins  in  soles  of  feet  and  fingers,  coldness,  itch- 
ing of  anus  and  scrotum  or  of  other  parts. 

Pain.     Short,  sharp,  cutting,  boring.     Deep  pain  ;  comes  in 


DISEASES   OF  THE   NERVOUS   SYSTEM.  29 

attacks,  one  second  to  one-half  minute  repeated,  or  in  severe 
attacks  for  several  hours  or  days  with  intermissions,  rarely  con- 
tinuous attacks.  Begins  in  thighs  and  legs.  Pain  is  a  prominent 
symptom  early,  but  may  continue  through  all  stages.  It  may  be 
mistaken  for  rheumatism  or  sciatica,  but  its  character  is  different. 
It  is  the  same  as  in  alcoholic  multiple  neuritis,  but  there  tender- 
ness exists.  There  is  no  relation  between  intensity  of  pain  and 
degree  of  ataxia.  As  disease  advances  upward  the  pains  extend. 
Pain  may  be  absent  or  insignificant  in  some  cases,  especially  in 
cases  beginning  with  optic-nerve  atrophy. 

Pain  in  the  small  of  the  back  and  loins  of  an  aching  character 
may  occur. 

Girdle  sensation  or  sensation  of  tightness  and  pressure  in- 
tense and  severe,  about  the  legs  and  body.  This  ascends  gradu- 
ally as  the  disease  advances. 

Loss  of  knee-jerk,  called  Westphal's  symptom. 

Imperfect  control  of  bladder.  Slow  urination.  Slight  drib- 
bling, and  hasty  urination.  Finally  control  is  very  imperfect  and 
may  be  painful.  This  may  be  a  dangerous  complication,  since 
death  from  cystitis  occurs. 

Impotence  ;  occasionally  priapism  and  sexual  excitement  pre- 
cedes this. 

Constipation  ;  usually  obstinate  throughout. 

Loss  of  pupil  reflex  to  light,  the  reaction  in  accommodation 
being  preserved —  Argyle-Robertson  pupil. 

Contracted  pupil,  "  myosis  spinalis,"  is  frequent  but  not 
constant. 

Symptoms  in  Stage  of  Ataxia. 

In  addition  to  those  of  first  stage  there  develop  : 

Anaesthesia  and  analgesia.  Sense  of  pain  impaired  and  de- 
layed. This  may  be  tested  with  faradic  brush.  It  prevents  in- 
juries from  being  perceived  ;  hence  ulcer  of  foot  and  Charcot 
joints  occur  as  complications.  Hence,  guard  against  accidents 
in  giving  hot  baths,  blisters,  etc. 

Hyperalgesia.  Sensation  of  pain  may  be  produced  by  any 
touch,  and  pain  is  felt  severely.  This  occurs  in  a  few  cases  early 
in  the  disease. 

Change  in  temperature  sensation.  Cold  felt  keenly  and  heat 
less  than  normal. 

Complete  anaesthesia  develops  late  in  the  disease  in  the  ex- 
tremities. 


30  DISEASES   OF   THE   NERVOUS   SYSTEM. 

Impairment  of  muscular  sense.  Muscular  sense  is  the  sense 
by  which  the  situation  and  movements  of  the  limbs  are  appreci- 
ated, and  pressure  and  weight  are  felt.  Not  same  as  effort  sense. 
Imperfect  perception  of  weight  and  pressure  is  a  symptom  ob- 
served late.  Situation  of  limbs  is  imperfectly  perceived.  Hence, 
one  means  of  perfect  guidance  of  limbs  is  removed.  Hence, 
patient  walks  badly  in  the  dark,  and  cannot  touch  objects  accu- 
rately with  eyes  closed  ;  hence,  he  watches  his  own  motions — aid- 
ing his  muscular  sense  by  sight.  Therefore  a  blind  ataxia  is  the 
most  helpless  of  all. 

Ataxia  is  imperfect  co-ordination  of  muscular  action.  For 
every  compound  act  a  regular  succession  and  proper  degree  of 
motions  are  needed,  e.g.,  closure  of  fist,  walking.  This  regula- 
tion is  largely  automatic  and  is  carried  on  in  subcortical  cen- 
tres, which  receive  unconscious  sensations  through  the  pos- 
terior nerve-roots.  It  may  be  voluntary,  by  an  effort  of  attention, 
and  is  so  at  first,  for  all  motion,  and  always  for  highly  complex 
motion,  e.g.,  writing.  Hence  ataxia  of  movement  may  occur  in 
many  diseases.  It  is  a  prominent  symptom  in  locomotor  ataxia. 

Romberg's  symptom — swaying  when  standing  with  eyes 
closed. 

Ataxic  gait — legs  wide  apart,  feet  lifted  too  high,  and  planted 
too  forcibly,  steps  being  of  irregular  length  and  body  imperfectly 
balanced. 

Imperfect  use  of  hands  in  dressing,  writing,  etc.  Irregular 
contraction  of  muscles  on  effort.  Imperfect  muscular  tone. 

Tests  of  ataxia.  Stand  with  eyes  closed,  walk,  turn  suddenly 
or  walk  backward  ;  touch  heel  to  toe,  or  heel  to  knee  ;  touch 
finger  to  nose  or  both  fingers  with  eyes  closed  ;  pick  up  pin  ; 
button  clothes. 

Symptoms  occasionally  present,  due  to  complication  of  neuritis  in 
various  nerves.  Optic  nerve  atrophy,  with  progressive  blindness 
develops  in  twenty  per  cent,  of  the  cases.  Optic  disc  looks  white, 
then  gray.  Arteries  appear  small  and  walls  thin.  Visual  field  is 
contracted  for  colors  and  for  light.  Finally  total  blindness  oc- 
curs. 

Paralysis  of  the  ocular  muscles. 

VI.  n.  paralysis  :  convergent  strabismus,  with  contracted 
pupil. 

III.  n.  paralysis  ;  divergent  strabismus,  with  dilated  pupil 
and  ptosis.  Nystagmus  rarely  occurs. 


DISEASES   OF  THE   NERVOUS   SYSTEM.  31 

Deafness  develops  in  a  few  cases  from  atrophy  of  auditory 
nerve. 

Crises — (i)  gastric  ;  sudden  vomiting  with  pain,  for  several 
hours,  even  for  days.  Great  prostration  follows.  Rectal  feeding 
necessary.  Intestinal  and  rectal  crises  with  diarrhoea  and  tenes- 
mus  have  been  observed.  (2)  Laryngeal  ;  sudden  severe  cough, 
with  spasm  of  larynx  and  suffocation.  (3)  Cardiac  ;  attacks  of 
angina  pectoris.  All  due  to  a  complicating  peripheral  neuritis 
in  pneumogastric  nerve.  These  symptoms  are  quite  exceptional. 

Trophic  disturbances  are  more  common  in  stage  of  ataxia. 

Charcot  joints.  Knee,  elbow,  ankle,  wrist.  Enormous  swell- 
ing with  effusion  without  pain.  Erosion  of  ends  of  bones  and 
destruction  of  articulation.  Due  to  injury. 

Perforating  ulcer  of  foot,  caused  by  a  corn,  or  a  subcutane- 
ous haemorrhage,  or  a  caries  of  bone  neglected. 

Rarefication  of  the  bones  with  production  of  fractures. 

Irregular  muscular  atrophies  develop  late  in  the  disease. 

Herpetic  eruptions  and  pemphigus. 

These  are  due  to  a  combination  of  causes,  chiefly  to  a  loss  of 
pain  sense  which  prevents  injuries  from  being  perceived,  or  to  a 
complicating  peripheral  neuritis. 

Symptoms  in  Stage  of  Paralysis. 

General  nutrition  remains  good,  but  ataxia  becomes  so  ex- 
treme as  to  render  patient  helpless  and  confine  him  to  bed. 

Control  of  bladder  completely  lost,  and  urine  dribbles  con- 
stantly. 

Accidents  produce  injuries,  and  trophic  disturbances  follow. 

Hence  patients  die  of  bedsores,  cystitis,  exhaustion,  or  of 
complicating  pneumonia. 

Course  of  the  disease  is  chronic  through  the  three  stages,  last- 
ing twenty  to  forty  years. 

Usual  mode  of  onset  is  with  pain,  loss  of  knee-jerk,  bladder 
trouble,  impotence,  and  ataxia. 

Occasional  modes  of  onset  :  (i)  blindness,  loss  of  knee-jerk, 
imperfect  gait,  numbness,  but  no  pain. 

(2)  Gastric  crises  at  intervals,  loss  of  knee-jerk,  then  pain  and 
ataxia. 

(3)  Various  forms  of  strabismus,  myosis,  then  ataxia  of  arms. 
There  are  remissions  in  the  symptoms  and  complications  may 

subside,  but  no  true  arrest  occurs  or  recovery,  after  the  stage  of 
ataxia  has  begun. 


32  DISEASES   OF   THE   NERVOUS   SYSTEM. 

Diagnosis.  Early,  by  means  of  pains,  fatigue,  loss  of  knee- 
jerk,  and  Argyle-Robertson  pupil.  Late,  by  ataxia  and  bladder 
disturbance. 

Diagnosis  from  multiple  neuritis.     See  page  8. 

Treatment.  Moderate  exercise,  avoiding  all  fatigue.  Good 
general  diet  without  special  restrictions,  which  weaken  patient. 
Spinal  douches,  tepid  or  cool,  never  extreme.  Massage.  Prac- 
tise in  fine  movements  to  overcome  ataxia.  Medicines — arsenic, 
nitrate  of  silver,  ergot. 

Treatment  of  pain  by  antipyrine,  etc.,  gelsemium,  opium,  fara- 
dization, hot  applications.  Of  crises  by  counter-irritation  and 
morphine.  Of  optic  atrophy  by  strychnine.  Of  trophic  disturb- 
ances by  rest  and  apparatus. 

COMBINED   SCLEROSIS. 

This  is  a  Sclerosis  of  the  Lateral  and  Posterior  Columns 
{rare). 

(1)  Congenital  cases.     FriedreicJis  Hereditary  Ataxia  is  due  to 
defective  development  of  the  lateral  and  posterior  columns.     It 
occurs  in  several  members  of  a  family,  and  is  hereditary. 

Symptoms. — As  the  children  grow  up  they  are  found  to  be 
awkward.  They  walk  badly,  and  do  not  use  arms  well.  Re- 
flexes are  lost,  exceptionally  exaggerated.  Dull  pains  in  legs, 
not  lightning  in  character.  No  bladder  symptoms,  and  no  trophic 
changes,  and  no  crises.  Ataxia  is  marked  and  goes  on  to  actual 
paralysis.  Speech  may  be  thick  and  nystagmus  present.  The 
condition  is  a  chronic  one  lasting  during  life. 

(2)  Acquired  cases.     Ataxic  Paraplegia  of  Gowers. 

Etiology. — Occurs  in  males  chiefly,  between  thirty  and  forty 
years  of  life.  Not  after  syphilis,  but  after  exposure  to  cold  or 
sexual  excess.  Possibly  after  concussion  of  spine. 

Symptoms. — Slow  onset  of  weakness  and  ataxia  together.  Un- 
due fatigue,  unsteady  gait.  Romberg  symptom.  Dull  pain  in 
back  and  legs,  no  lightning  pains.  Reflexes  increased.  Knee- 
jerk  high,  ankle  clonus  present.  Sexual  power  lost.  Sphincters 
less  impaired  than  in  tabes.  Eye  symptoms  very  rare.  Tremor 
of  face  and  speech  sometimes  develops. 

Differs  from  tabes  in  fact  that  the  nerve-roots  are  not  in- 
volved. 

Course. — Weakness  increases   slowly    to   paralysis.     Rigidity 


DISEASES   OF   THE   NERVOUS   SYSTEM.  33 

soon  develops,  and  contractures.     Death  occurs  from  complica- 
tions. 

THE  ASSOCIATION  COLUMNS. 

8.  Antero- Lateral  Column. — There  is  a  large  collection  of  nerve- 
fibres  forming  a  white  column  lying  adjacent  to  the.  gray  matter 
of  the  cord,  in  front  and  inside  of  the  pyramidal  tract,  and  inside 
of  the  direct  cerebellar  and  antero-lateral   ascending  tracts,  ex- 
tending as  far  forward  as  the  anterior  nerve-roots.     A   portion 
lying  next  to  the  gray  matter  has  been  named  the  lateral  limiting 
layer.     This  column  contains  a  few  fibres  which  degenerate  all 
the  way  upward   to   the  medulla,  and  it  is   possible  that  some 
sensory  impulses  are  transmitted  through  it.     The  major  part  of 
the  fibres  are,  however,  short,  and  serve  to  connect  the  various 
segments  of  the  cord  with  one  another.     In  it  pass  the  majority 
of  the  "  association  fibres  "  of  the  cord  which  harmonize  the  ac- 
tion of  different  parts. 

9.  Anterior  Column. — This  lies  between  the  exit  of  the  anterior 
nerve  roots  and  the  anterior   median  column.     It   has   the  same 
function   as  the  antero-lateral   column,  and  like  it  ends  in  the 
formatio  reticularis  of  the  medulla. 

There  are  very  many  polygonal  cells  scattered  through  the 
gray  matter  in  both  horns  and  in  the  central  gray  which  send  out 
to  these  columns  an  axis  cylinder  process  which,  on  entering  the 
column  bifurcates,  sending  one  branch  down  and  the  other  upward. 
These  branches  give  off  collaterals  in  their  course  which  pass 
into  the  gray  matter  at  various  levels  and  terminate  in  brush-like 
expansions.  The  original  branches  terminate  in  the  same  way 
after  having  a  longer  or  shorter  course.  Thus  the  majority  of  the 
fibres  in  these  columns  are  true  association  fibres.  There  are  a 
few  such  fibres  also  in  the  portion  of  the  posterior  columns  ad- 
jacent to  the  gray  commissure. 

SECONDARY  DEGENERATIONS. 

When  the  cord  is  divided  by  an  injury  or  by  transverse  my- 
elitis there  results  a  degeneration  in  the  various  columns. 

The  anterior  median  and  lateral  pyramidal  columns  degenerate 
downward  for  their  entire  length.  There  is  also  a  short  tract  of 
degeneration  downward  in  the  lateral  zone  of  the  column  of  Bur- 


34  DISEASES   OF   THE   NERVOUS   SYSTEM. 

dach.     The  anterior  and  antero-lateral  columns  degenerate  down- 
ward for  a  short  distance. 

The  columns  of  Burdach  and  Goll  and  Cowers  and  the  direct 
cerebellar  column  degenerate  upward  through  their  entire 
length.  The  columns  of  Lissauer  and  the  anterior  and  antero- 

D 

lateral  columns  degenerate  upward  for  a  short  distance. 

Such  degenerations  are  due  to  the  fact  that  the  transverse 
lesion  cuts  off  the  individual  fibres  from  their  nutrient  cells,  and 
hence  the  distal  end  degenerates,  the  fibres  nourished  by  cells 
above  the  lesion  degenerating  downward  and  those  by  cells  be- 
low the  lesion  degenerating  upward. 

MYELITIS. 

This  is  an  inflammation  of  the  spinal  cord  involving  an  entire 
segment,  both  gray  and  white  matter. 

Pathology. — Cord  looks  normal,  but  feels  soft  at  points  ;  or 
may  break  in  two  and  be  soft  enough  to  be  fluid.  On  cutting  it 
the  cut  surface  swells  out  as  if  semi-fluid  ;  the  gray  matter  looks 
red  and  capillary  hemorrhages  are  seen  ;  the  limit  of  white  and 
gray  is  indistinct. 

Microscopically. — Large  numbers  of  inflammatory  corpuscles 
everywhere.  Nerve-cells  and  fibres  swollen  and  degenerated, 
granular  and  disappearing  or  atrophied.  Neuroglia  cells  in- 
creased. Deiter's  spider  cells  present.  Fatty  and  granular  cells 
everywhere  as  evidence  of  degeneration.  Vessels  are  distended 
with  blood  and  ruptured;  walls  may  be  infiltrated  and  thickened- 

Secondary  degeneration  as  already  enumerated. 

Etiology. — Males  more  than  females.  Soldiers,  porters.  Age 
ten  to  forty.  Exposure  to  cold.  Over  -  exertion.  Falls  and 
blows.  Concussion  of  cord.  Sexual  excesses.  Menstrual  sup- 
pression. After  confinement.  Injuries  of  the  cord.  Compres- 
sion of  the  cord  by  disease  of  spinal  bones  or  tumors.  Secondary 
to  acute  infectious  diseases.  Syphilis  and  chronic  alcoholism. 

Varieties,  General. — Entire  cord  affected — ascending  or  de- 
scending. 

Disseminated. — Various  segments  at  different  levels  affected. 

Transverse. — One  or  two  segments  at  one  level  affected. 

Symptoms. — (i)  Direct,  due  to  destruction  of  cord  tissue. 

i.  Motor.  Paralysis,  atrophy.  R.  D.  Loss  of  tone  in  mus- 
cles. 


DISEASES   OF   THE   NERVOUS   SYSTEM.  35 

2.  Reflex.     Loss  of  spinal  reflexes.     Paralysis  of  the  bladder 
and  rectum,  impotence. 

3.  Sensory.      Numbness.       Pain.      Paraesthesia,    anaesthesia. 
Hyperaesthesia  at  upper  level  of  lesion.     Pain  and  tenderness  of 
back  to  heat. 

4.  Vaso-motor   and    trophic.      Imperfect    circulation.      Skin 
cold.     Sweat  profuse.     Bed-sores  on  buttocks,  sacrum,  and  heels. 

The  distribution  of  the  direct  symptoms  depends  on  the  ex- 
tent of  the  lesion.  If  general  they  are  universal.  If  dissemi- 
nated they  are  scattered.  If  transverse  they  are  limited  to  one 
level. 

Diagnosis  of  level  from  situation  of  symptoms,  motor  or  'sen- 
sory, see  table,  page  10. 

Symptoms. — (2)  Indirect,  due  to  cutting  off  of  impulses  to  other 
parts.  The  cord  transmits  impulses  to  and  from  the  brain.  In 
disseminated  and  transverse  myelitis  tracts  are  broken,  (i)  Mo- 
tor tracts  to  parts  below,  hence  secondary  lateral  sclerosis  with 
its  symptoms.  (2)  Sensory  tracts  from  parts  below,  hence  sec- 
ondary degenerations  upward  with  their  symptoms. 

Secondary  symptoms  are  : 

1.  Rigidity  and  increased  reflexes,  contractures,  spasms  of  legs, 
paralyzed  muscles  not  atrophied  and  no  R.  D. 

2.  Loss  of  bladder  control  without  bladder  paralysis,  priap- 
istn. 

3.  Imperfect  sensation  without  incoordination. 

4.  Imperfect  perception  of  pain,  hence   bed-sores  from  dirt, 
bed-sores  over  sacrum,  glutei,  heels,  and  ankles. 

Examples  :  In  general  myelitis,  direct  symptoms  throughout 
body. 

In  disseminated  myelitis,  direct  symptoms  in  irregular  areas, 
few  indirect  symptoms. 

In  transverse  myelitis,  direct  symptoms  very  limited,  indirect 
symptoms  below  the  lesion. 

(a)  Cervical  transverse  myelitis,  direct  symptoms  in   arms,  in- 
direct in  legs. 

(b)  Dorsal  transverse  myelitis,  direct  symptoms  few,  in  trunk, 
indirect  in  legs,  arms  free. 

(c)  Lumbar  transverse  myelitis,  direct  symptoms  in  legs,  arms 
free,  no  indirect  symptoms. 

Course  of  General  Myelitis  and  Disseminated  Myelitis. — Acute  or 
subacute,  onset  in  two  weeks  after  a  cold  or  great  strain  or  after 


36  DISEASES   OF   THE   NERVOUS   SYSTEM. 

typhus,  typhoid,  small-pox,  confinement,  syphilis.  Weakness  in 
limbs.  Pains  in  back  and  limbs.  Prostration.  Then  paralysis. 
Pain  and  anaesthesia.  Bladder  and  rectal  symptoms.  Then  pa- 
tient is  confined  to  bed  and  bed-sores  develop.  Slow  course  for 
a  year  to  three  years  and  occasionally  gradual,  imperfect  recov- 
ery. Usually  cystitis,  bed-sores,  or  pneumonia  and  death. 

Course  of  Transverse  Myelitis. — Acute,  onset  after  injury — blow, 
fall,  wound,  dislocation  of  spine,  or  strain,  causing  hemorrhage 
in  cord  ;  or  from  embolism  of  spinal  arteries. 

Chronic,  onset  after  spinal  caries  with  deformity  and  press- 
ure, or  tumor  in  spinal  canal  or  cord.  Course  depends  on  pos- 
sibility of  removing  the  cause. 

Diagnosis. — Myelitis  vs.  multiple  neuritis,  see  page  8. 

MYELITIS  vs.  MENINGITIS. 

Very  rapid  onset.  Slower  onset. 

Fever  moderate.  Fever  high. 

Pain  in  back  moderate,  in  limbs  or  body  Pain  in  back  and  body  and  limbs  very  se- 

dull.  vere,  increased  by  motion. 

Hyperaesthesia  slight  in  a  band  at  upper  Hypersesthesia  of  entire  body  and  limbs 

level  of  lesion.  very  intense. 

Anaesthesia  below  lesion.  No  anaesthesia. 

No  spasms  or  rigidity.  Spasms  of  limbs  and  back  with  rigidity  of 

back  appear  early. 

Paralysis   total  in   some    muscles  with  Paralysis    only  apparent ;  due  to  fear  of 

atrophy  and  R.  D.  pain  on  motion  ;  no  atrophy. 

Sphincters  paralyzed.  Sphincters  not  affected. 

Bed-sores  and  cystitis.  No  bed-sores  or  cystitis. 

MYELITIS  vs.          HYSTERICAL  PARAPLEGIA. 

Anaesthesia  below  lesion  includes  geni-  Anaesthesia  varies  in  level  and  genitals 

tals.  never  included. 

If  thighs  are  paralyzed  and  atrophied  re-  When  legs  are  paralyzed  reflexes  are  ex- 
flexes  are  lost.  aggerated. 

Usually  some  muscles  atrophy  and  show  Muscles  rarely  atrophy  and  R.  D.  never 

R-  D.  appears. 

Sphincters  usually  involved.  Sphincters  rarely  involved. 

Diagnosis  of  level  of  lesion  by  distribution  of  anaesthesia,  see 
table,  page  10. 

Treatment  of  myelitis. 

When  onset  is  acute  remove  cause,  and  use  counter-irritation, 
ice-bag  or  warm  douche.  Keep  at  perfect  rest  in  prone  posi- 


DISEASES   OF  THE  NERVOUS   SYSTEM.  37 

tion.  Give  sedatives  and  ergot,  in  early  stage  give  purgatives, 
calomel,  or  salts. 

When  case  is  chronic  in  onset  or  in  course  : 

Employ  counter-irritation.  Cups,  blisters,  cautery,  ether 
spray  ;  but  not  in  cases  with  tendency  to  bed-sores. 

Use  baths,  douches,  tepid  and  cold,  to  spine. 

Keep  up  strength  of  patient  by  good  diet,  and  regulate  diges- 
tion. 

Use  massage  to  the  limbs— hot  baths  for  rigidity. 

Use  interrupted  galvanic  current  to  atrophied  and  paralyzed 
muscles. 

Prevent  cystitis  by  keeping  catheters  and  parts  clean  and 
aseptic. 

Prevent  bed-sores  by  careful  padding  or  water-bed,  by  spong- 
ing with  alcohol  and  alum-water. 

Treat  cystitis  by  washing  out  the  bladder  as  in  surgery. 

Treat  bed-sores  by  aseptic  dressings,  as  in  surgery. 

For  pain  apply  heat  or  faradic  brush  to  part.  Give  anti- 
pyrin,  antifebrin,  phenacetine,  morphine,  salicin,  salicylic  acid. 

For  spasms  apply  heat  to  spine,  or  hot  bath  to  legs,  or  cups. 
Give  bromides. 

For  rigidity,  when  beginning,  pads  and  massage. 

For  incontinence  of  urine  pads  of  absorbent  cotton,  or  wear 
urinal. 

Medicines  in  chronic  myelitis  : 

Iodide  of  potash,  gr.  x.  to  xx.,  t.i.d. 

Nitrate  of  silver  in  pill  with  kaolin,  gr.  %  t.i.d.  increased. 

Ergotin  when  congestion  is  suspected. 

Strychnine  when  an  increase  of  reflex  activity  is  not  present. 

Phosphorus  and  arsenic  as  nerve-tonics. 

Use  ung.  hydrarg,  and  KI  in  large  doses  in  syphilitic  cases. 

HEMORRHAGE   INTO   THE   SPINAL   CORD. 

Hemorrhage  into  the  spinal  cord  or  into  the  membranes  is  a 
rare  occurrence,  and  is  almost  always  due  to  traumatism.  The 
symptoms  produced  are  those  of  sudden  suspension  of  all  spinal 
functions  at  and  below  the  level  of  the  hemorrhage.  They  are 
therefore  identical  with  those  of  transverse  myelitis,  and  the  sud- 
den onset  affords  the  only  means  of  distinguishing  the  two  dis- 
eases. 


38  DISEASES   OF   THE   NERVOUS   SYSTEM. 


TUMORS  OF  THE   SPINAL   CORD. 

Tumors  rarely  grow  in  the  spinal  cord.  They  are  usually 
secondary  to  tumors  elsewhere.  All  varieties  may  occur.  The 
symptoms  produced  are  those  of  transverse  myelitis  of  slow  onset 
and  characterized  by  extreme  pain  at  the  level  of  the  tumor  or  in 
the  sensory  areas  which  correspond  to  the  segment  in  which  the 
tumor  grows..  The  only  relief  is. by  operation. 

BROWN-SEQUARD'S    PARALYSIS. 

Hemorrhages  in  the  cord,  tumors  in  or  about  the  cord,  and 
bony  growths  or  callous,  the  result  of  injury,  sometimes  divide  or 
compress  one-half  only  of  the  cord.  The  symptoms  resulting  were 
first  described  by  Brown-Se'quard,  and  hence  the  condition  lias 
been  named  after  him.  This  condition  is  as  follows  :  (i)  on  the 
side  of  the  lesion  there  is  paralysis  with  increased  reflexes,  and 
sometimes  a  loss  of  muscular  sense  below  the  level  affected,  and 
a  marked  hyperaesthesia  to  touch  and  pain  ;  (2)  on  the  side  op- 
posite to  the  lesion  there  is  no  paralysis,  but  there  is  a  loss  of 
sensation  of  touch,  temperature,  and  pain,  and  sometimes  a  de- 
velopment of  bed-sores  below  the  level  of  the  lesion  ;  (3)  at  the 
level  of  the  lesion  there  is  a  band  about  the  body  of  anaesthesia, 
with  another  band  of  hyperaesthesia  above  it ;  the  band  on  the 
side  of  the  lesion  being  a  little  higher  than  upon  the  opposite 
side. 


THE   BRAIN   AND    ITS    DISEASES. 
I.  THE  CORTEX  OF  THE  CEREBRAL  HEMISPHERES. 

THE  cortex  consists  of  gray  matter  spread  out  in  a  layer  over 
the  cerebral  hemispheres,  3  mm.  thick  and  about  200,000  sq.  mm. 
in  extent  ;  its  amount  varying  greatly  in  different  persons  ;  its 
development  determining  mental  capacity.  The  development  of 
fissures  throwing  the  cortex  into  folds  enables  this  large  extent 
to  be  contained  in  the  skull. 

The  Microscopic  Appearance  of  the  Cortex. — Cells  arranged  in 
layers. 

(1)  Superficial   or   molecular    layer   (T17)    small   cells.     Much 
neuroglia. 

(2)  Layer  of  small  pyramids   (-j^)  with    many    branches  and 
short  process. 

(3)  Layer  of  large   pyramids  (^)   with  few  branches  and  a 
long  projection  fibre  process. 

(4)  Layer    of    polymorphous    cells    (-fo)    with     many    short 
branches  and  a  short  process. 

(5)  Layer  of  fusiform  cells  (T2ff)  with  short  branches  and  asso- 
ciation fibre  process. 

Fibres  traverse  these  layers  giving  off  collaterals  and  form  an 
intricate  net-work  throughout  the  gray  matter.  There  are  great 
variations  in  the  structure  of  different  regions.  (See  "  Ouain's 
Anatomy,"  loth  Ed.,  Vol.  III.) 

The  fibres  arising  from  the  cortex  and  constituting  the  white 

o  o 

matter  beneath  it  are  (i)  association  fibres  passing  to  some  other 
part  of  the  cortex  ;  (2)  commissural  fibres  passing  to  the  cortex 
of  the  opposite  hemisphere  ;  (3)  projection  fibres  passing  to  the 
basal  ganglia,  cerebral  axis  or  spinal  cord. 

Divisions  of  the  Cortex  into  Lobes  and  Convolutions. — Frontal 
lobe,  40  per  cent.  ;  parietal  lobe,  20  per  cent.  ;  temporal  lobe, 
20  per  cent.;  occipital  lobe,  17  per  cent.;  Island  of  Reil,  3  per 
cent,  of  extent  of  cortex. 

Landmarks  on  the  Cortex. — Fissure  of  Sylvius,    fissure  of  Ro- 


40  DISEASES  OF  THE  NERVOUS  SYSTEM. 

lando,    iflterparietal    fissure,    parieto-occipital    sulcus,    calcarine 
fissure,  eolloso-marginal  fissure. 

CRANIOCEREBRAL  TOPOGRAPHY. 

To  find  the  fissure  of  Rolando,  lay  down  a  line  from  the  root 
of  the  nose  to  the  occipital  protuberance  over  the  top  of  the 
head  and  take  a  point  0.557  of  the  distance  back  upon  tins  line. 
This  point  will  correspond  to  the  upper  end  of  the  fissure.  The 
fissure  makes  an  angle  of  67°  with  the  median  line  just  meas- 
ured. Hence  if  two  strips  of  metal,  fixed  to  one  another  at  this 
angle  be  placed  on  the  head  with  their  junction  upon  the  upper 
end  of  the  fissure,  when  one  strip  is  on  the  median  line  the  other 
strip,  pointing  forward  and  downward,  must  lie  over  the  fissure 
of  Rolando.  In  its  lower  third  the  fissure  becomes  a  little  more 
vertical  than  the  strip.  The  fissure  is  about  three  and  a  half 
inches  long. 

To  find  the  fissure  of  Sylvius,  lay  down  a  base  line  from  the 
lower  margin  of  the  orbit  to  the  auditory  meatus.  Lay  down  a 
second  line  parallel  to  the  base  line  from  the  external  angular 
process  of  the  frontal  bone  backward  one  inch  and  a  quarter  and 
then  measure  upward  one  quarter  of  an  inch  ;  this  gives  point 
one.  Find  the  most  prominent  part  of  the  parietal  eminence 
and  from  it  draw  a  line  downward  perpendicular  to  the  base 
line,  and  on  this  take  a  point  three-quarters  of  an  incli  below 
the  eminence  ;  this  gives  point  two.  Join  these  two  points  and 
the  line  will  lie  over  the  fissure  of  Sylvius.  The  anterior  limb  of 
the  fissure  will  be  two  inches  behind  the  external  angular  proc- 
ess. The  fissure  of  Sylvius  is  about  four  inches  long. 

To  find  the  parieto-occipital  fissure,  continue  the  line  of  the 
fissure  of  Sylvius  to  the  median  line.  At  their  junction  lies  this 
fissure.  Since  all  areas  now  open  to  surgical  operation  can  be 
located  with  a  definite  relation  to  these  three  fissures,  no  further 
rules  are  necessary.  Since  in  opening  the  skull  it  is  customary 
to  make  a  fenestra  of  at  least  an  inch  in  diameter,  and  it  is  fre- 
quently necessary  to  enlarge  the  opening  much  more,  a  proced- 
ure in  no  way  dangerous  under  aseptic  conditions,  there  is  no 
difficulty  in  recognizing  the  fissures  and  convolutions  exposed  if 
the  rules  are  closely  followed.  Prior  to  the  large  incision  of  the 
scalp  it  is  well  to  mark  certain  points  upon  the  skull  by  the 
sharp  point  of  a  chisel,  so  that  when  the  bone  is  laid  bare  sur- 
face landmarks  may  still  be  kept  in  view. 


DISEASES   OF   THE   NERVOUS   SYSTEM.  41 


LOCALIZATION  OF  FUNCTIONS  IN  THE  CORTEX. 

Proofs  from  comparative  anatomy  ;  natural  and  experimental 
atrophy  ;  process  of  development  ;  irritation  and  excision  of 
cortex  with  various  results  ;  pathological  lesions  of  limited  ex- 
tent with  secondary  degenerations. 

The  functions  of  the  cortex  in  general  are  : 

(1)  To  receive  impressions  from  the  various  sensory  organs 
as  conscious  perceptions. 

(2)  To  associate  these  various  simultaneous  perceptions  into 
a  mental  image  or  concept. 

(3)  To  retain  these  concepts  as  memories  so  that  objects  can 
be  recognized  or  recalled. 

(4)  To  give  expression  to  thought  in  action  and  in  speech. 

(5)  To  restrain  the  flow  of  thought  and  to  inhibit  or  control 
automatic  and  reflex  acts. 

It  has  been  established  that  various  powers  of  perception, 
memory,  and  volition  can  be  definitely  assigned  to  various  parts 
of  the  brain  ;  that  each  sense  has  its  corresponding  area  in  the 
cortex  and  each  voluntary  movement  its  point  of  departure  from 
the  cortex. 

It  has  been  proven  that  perceptions  leave  behind  them  a  phys- 
ical trace  inseparably  connected  with  the  area  in  which  they 
were  originally  received  ;  that  irritation  of  this  area  produces  a 
renewal  in  consciousness  of  the  original  perception  as  a  memory, 
which  may  be  so  vivid  as  to  appear  real,  being  then  a  halluci- 
nation ;  that  destruction  of  this  area  causes  a  loss  of  the  power 
of  recalling  the  previous  perception  or  of  recognizing  it  when 
repeated. 

It  has  been  proven  that  movements  which  are  acquired  by 
practice,  and  are  therefore  the  result  of  conscious  effort,  are 
always  initiated  from  a  definite  area  ;  that  this  area  is  insepar- 
ably related  to  movements  ;  since  its  irritation,  by  any  cause, 
results  in  the  production  of  forcible  movements  of  the  nature  of 
spasms  and  its  destruction  produces  a  loss  of  the  power  of  move- 
ment or  paralysis  of  voluntary  action. 

It  has  been  proven  that  the  use  of  language  involves  both  the 
recollection  of  auditory  and  visual  symbols  and  the  initiation  of 
impulses  of  speech  and  writing,  thus  calling  into  play  not  only 
the  motor  portion  of  the  brain,  destruction  of  which  therefore 


42  DISEASES   OF  THE   NERVOUS   SYSTEM. 

causes  a  loss  of  speech,  but  also  the  sensory  portion  of  the  brain, 
a  lesion  of  which  will  also  cause  aphasia. 

There  are  certain  areas  upon  the  cortex  of  the  brain,  not 
necessarily  coextensive  with  either  lobes  or  convolutions,  whose 
functions  are  accurately  known. 

These  areas  are  :  (i)  The  sensori-motor  area.  (2)  The  visual 
area.  (3)  The  auditory  area.  (4)  The  area  of  sensations  of 
smell  and  of  taste.  (5)  The  speech  areas. 

THE  SENSORI-MOTOR  AREA. 

The  sensori-motor  area  includes  the  cortex  of  the  anterior  and 
posterior  central  convolutions  which  border  the  fissure  of  Ro- 
lando and  the  adjacent  cortex  in  front  and  behind  these  convolu- 
tions. Each  hemisphere  controls  movement  on  the  opposite  side 
of  the  body,  but  as  the  right  hand  is  more  generally  used  and  is 
better  trained  than  the  left,  this  area  is  larger  on  the  left  hemi- 
sphere than  on  the  right. 

The  cortex  of  the  posterior  part  of  the  second  frontal  convo- 
lution controls  the  movements  of  the  eyes  and  head.  Impulses 
starting  from  this  area  produce  conjugate  movement  of  these 
parts  toward  the  opposite  side.  The  eye  district  is  below,  the 
head  district  above. 

The  lower  third  of  the  anterior  and  posterior  central  convolu- 
tions governs  the  movements  of  the  face,  tongue,  larynx,  and 
pharynx.  The  eyebrows  and  cheeks  are  controlled  by  the  upper 
and  forward  part  of  this  area  ;  the  tongue  and  larynx  by  the 
lower  and  forward  part  ;  the  mouth,  pharynx,  and  platysma  by 
the  hinder  part. 

The  middle  third  of  the  anterior  and  posterior  central  convo- 
lutions governs  the  movements  of  the  upper  extremity ;  the 
shoulder  motions  being  controlled  in  the  anterior  and  upper 
part  of  this  area;  the  elbow  motions  in  its  middle  part  and  the 
hand  and  finger  motions  in  its  posterior  and  lower  part. 

The  upper  third  of  the  anterior  and  posterior  central  convo- 
lutions, including  their  junction  in  the  para-central  lobule,  con- 
trols the  motions  of  the  lower  extremity,  the  thigh,  knee,  foot, 
and  toes  being  governed  by  various  parts  of  this  area  from  be- 
fore backward  in  the  order  named. 

The  parts  susceptible  of  the  finest  and  most  delicate  move- 
ments, those  directed  by  the  most  acute  sensations,  the  lips,  the 


DISEASES   OF   THE   NERVOUS   SYSTEM.  43 

fingers,  and  the  toes,  lie  furthest  back  in  the  motor  area,  chiefly 
in  the  posterior  central  convolution.  Lesions  in  this  convolution 
almost  always  cause  some  loss  of  tactile  sensation  as  well  as 
paralysis,  and  hence  this  area  is  thought  to  be  the  seat  of  tactile 
sensations  as  well  as  of  movements,  while  some  cases  point  to 
the  localization  of  muscular  sensations  in  the  area  just  behind 
that  of  motion. 

The  median  surface  of  the  hemisphere  in  front  of  the  para- 
central  lobule  is  known  to  be  related  to  movements  of  the  trunk 
in  monkeys,  but  the  cortex  in  front  of  the  leg  area  on  the  con- 
vexity is  the  probable  location  of  the  trunk  area  in  man. 

There  are  no  sharply  defined  sections  of  the  motor  area  to  be 
assigned  to  special  motions.  Eacli  motion,  each  part  of  a  limb, 
has  a  wide  general  representation  over  the  cortex  and  a  special 
representation  at  a  limited  area.  The  areas  of  representation  of 
different  limbs  merge  into  one  another  ;  thus,  in  the  representa- 
tion of  the  thumb  we  find  that  there  is  a  focus,  but  that  the 
thumb  is  represented  over  a  great  deal  of  the  upper  limb  region, 
and  that  this  representation  diminishes  in  intensity  gradually  as 
we  pass  from  the  focus  \ipward.  This  explains  the  fact  that  the 
excision  of  a  small  area  does  not  totally  paralyze  the  portion  of 
the  limb  represented  chiefly  on  that  area.  The  adjacent  areas 
represent  to  some  extent  that  limb,  and  hence  can  govern  it  if 
need  be. 

The  motor  centres  govern  motor  acts  rather  than  special 
muscles,  each  act  involving  a  succession  of  movements  of  differ- 
ent joints  by  various  groups  of  muscles. 

Cortical  Spasm  and  Paralysis. — Irritation  in  the  motor  area 
produced  by  any  kind  of  disease  gives  rise  to  localized  spasms 
or  convulsions,  called  Jacksonian  epilepsy.  Destruction  of  the 
motor  area  gives  rise  to  paralysis.  The  point  of  beginning  of 
the  spasm  or  the  extent  of  paralysis  depends  on  the  part  of  the 
motor  area  diseased.  Hence,  from  the  character  of  either  of 
these  symptoms  a  conclusion  can  be  reached  as  to  the  location 
of  the  disease.  Cortical  spasm  or  paralysis  usually  begins  in  the 
face  or  in  one  limb  of  one  side  and  extends.  The  order  of  the 
progress  also  indicates  the  location  of  the  disease,  e.g.,  from  face 
to  arm,  then  to  leg,  or,  vice  versa,  e.g.,  spasm  of  shoulder,  arm  and 
hand,  vs.  spasm  of  fingers,  arm,  and  shoulder  :  the  disease  is 
most  intense  in  the  part  first  affected.  Sensations  of  numbness 
precede  the  spasm.  A  cortical  spasm  begins  locally,  and  usually 


44  DISEASES   OF  THE   NERVOUS   SYSTEM. 

extends  until  one  side  of  the  body  is  affected.     It  is  usually  fol- 
lowed by  temporary  weakness.     Consciousness  is  preserved. 

Cortical  paralysis  is  monoplegic  in  type  vs.  subcortical  paral- 
ysis, which  is  hemiplegic  in  type.  A  slowly  advancing  paralysis 
indicates  a  slowly  extending  destruction  of  tissue.  Cortical 
paralysis  is  associated  with  increased  reflexes,  but  there  is  no 
atrophy  and  no  change  in  electric  reactions.  Contractures  de- 
velop late. 

THE  VISUAL  AREA. 

The  area  of  sensations  of  sight  is  located  in  the  occipital  lobe  of 
the  brain,  including  the  cuneus  on  the  median  surface  and  the 
occipital  convolutions  on  the  convexity.  The  cortex  lying  in  the 
calcarine  fissure  is  the  part  primarily  reached  by  the  visual  im- 
pulses, but  the  parts  named  are  also  concerned  in  vision.  Each 
occipital  lobe  receives  impressions  from  one-half  of  both  eyes, 
hence  a  lesion  in  one  lobe  produces  hemianopsia,  a  half-blind- 
ness in  both  eyes,  the  blind  field  of  vision  being  on  the  opposite 
side  to  the  lesion.  This  is  termed  homonymous  hemianopsia, 
that  is,  a  blindness  in  the  like  named  halves  of  both  visual  fields. 
When  the  right  occipital  lobe  is  affected  the  patient  cannot  see 
anything  on  the  left  side  of  the  middle  line  as  he  looks  forward. 

Irritation  of  the  occipital  lobe  may  cause  hallucinations  of 
light  or  even  of  objects  which  are  referred  to  the  opposite  visual 
field.  Destruction  of  the  occipital  lobe  on  the  left  side  destroys 
sight  memory  pictures,  hence  recognition  of  things  seen  may  be 
impossible,  and  reading  power  may  be  lost. 


THE  AUDITORY  AREA. 

The  area  of  sensations  of  sound  is  located  in  the  first  and  second 
temporal  convolutions  of  the  brain.  Each  ear  is  connected  with 
both  hemispheres  ;  hence  deafness  from  a  unilateral  lesion  is 
only  partial  and  is  not  generally  noticed.  But  if  both  temporal 
lobes  are  destroyed  the  patient  becomes  totally  deaf.  Irritation 
of  the  temporal  cortex  may  cause  hallucinations  of  hearing. 
This  may  be  the  first  symptom  of  a  convulsion  whose  origin  is 
an  irritation  in  this  part  of  the  cortex.  Destruction  of  the  tem- 
poral cortex  on  the  left  side  causes  word  deafness.  (See  speech 
areas.) 


DISEASES   OF  THE   NERVOUS   SYSTEM.  45 


THE  SMELL  AND  TASTE  AREA. 

The  area  of  sensations  of  smell  and  taste  is  located  at  the  tip  of 
the  temporal  lobe  on  its  under  and  inner  surface,  which  rests  on 
the  sphenoid  bone.  Each  lobe  is  related  to  sensory  organs  on 
both  sides,  and  a  unilateral  lesion  does  not  often  produce  notice- 
able symptoms. 

THE  SPEECH  AREAS  AND  APHASIA. 

The  speech  areas  are  of  four  kinds  and  in  four  locations. 
They  are  limited  to  the  left  hemisphere  in  right-handed  persons 
and  to  the  right  hemisphere  in  left-handed  persons.  There  is  the 
motor  speech  area  in  the  posterior  part  of  the  third  frontal  convo- 
lution (Broca's  convolution),  in  which  the  movements  concerned 
in  the  act  of  speaking  are  controlled.  The  use  of  language  and 
the  power  of  talking  are  affected  when  this  region  is  destroyed. 
There  is  the  auditory  speech  area  in  the  first  and  second  temporal 
convolutions,  in  which  the  memories  of  word-sounds  are  stored  up. 
The  understanding  of  language  and  the  power  of  recollecting 
the  names  of  objects  are  lost  when  this  region  is  destroyed. 
There  is  the  visual  speech  area  in  the  occipital  and  lower  parietal 
region,  in  which  the  memories  of  printed  words  are  stored  up. 
The  understanding  of  written  language  and  the  power  to  read 
are  lost  when  this  region  is  destroyed.  The  power  of  writing  is  a 
part  of  speech  and  is  usually  lost  when  the  motor  speech  area  is 
destroyed,  but  its  exact  location  is  not  fully  determined  ;  some 
cases  pointing  to  the  second  frontal  convolution,  others  to  the 
lower  parietal  convolution  near  the  hand  centre  as  its  probable 
cortical  position. 

It  is  accepted  that  every  word  in  ordinary  use  has  a  complex 
mental  substratum,  which  may  be  termed  the  word-image,  made 
up  of  a  number  of  memory-pictures.  The  memory  of  the  sound 
of  a  word  as  spoken,  the  memory  of  the  appearance  of  the  word 
as  printed,  the  memory  of  the  muscular  movements  needed  to 
write  the  word  or  to  pronounce  it,  are  known  to  be  distinct  from 
one  another  and  yet  to  be  associated  together.  Loss  of  one  of 
these  memory-pictures,  or  disturbance  in  their  association,  im- 
pairs the  integrity  of  the  word-image,  and  produces  such  de- 
fects in  its  use  as  are  indicated  by  the  names  given  to  the  re- 
spective varieties  of  aphasia.  A  division  of  disturbances  of 


46  DISEASES   OF   THE   NERVOUS   SYSTEM. 

speech  has  been  made  into  two  great  classes  of  sensory  and 
motor  aphasia — the  first  due  to  defect  in  the  receptive,  and  the 
second  due  to  impairment  of  the  emissive  functions  of  the  brain. 
A  further  subdivision  into  several  varieties  has  been  made. 
These  are  word-deafness,  word-blindness,  agraphia,  motor  apha- 
sia, and  paraphasia.  But,  before  considering  these  defects,  let 
us  look  at  the  physical  basis  of  the  thought  which  lies  back  of 
the  word.  Take  the  idea  "  bell "  as  an  example. 

The  idea  of  a  bell  is  made  up  of  separate  memory-pictures  of 
its  shape,  size,  color  (visual  picture)  ;  weight  (muscular  sense 
picture)  ;  cold  smooth  surface  (touch  picture)  ;  and  sound  (au- 
ditory picture).  These  various  memories,  received  by  different 
senses  and  stored  up  in  different  parts  of  the  cortex,  are  asso- 
ciated together  in  a  mental  image  of  the  object  bell. 

To  this  mental  image  the  word  image  is  added  of  the  word 
bell  as  heard,  as  printed,  as  spoken,  as  written,  making  up  a  con- 
geries of  memory-pictures  forming  a  "  concept."  Any  one  of 
these  memory-pictures  may  be  lost  by  disease.  If  the  memories 
of  the  object  are  lost  the  symptom  is  called  apraxia.  If  the 
memories  of  the  word  are  lost  the  symptom  is  called  aphasia. 

To  examine  an  aphasic  thoroughly  it  is  necessary  to  test — 

1.  The  power  to  recognize  objects  seen,  heard,  felt,  tasted,  or 
smelt,  and  their  use. 

This  will  determine  whether  the  condition  of  apraxia  is  pres- 
ent. 

2.  The  power  to  recall  the  spoken  name  of  objects  seen,  heard, 
handled,  tasted,  or  smelt. 

3.  The  power  to  understand  speech  and  musical  tunes. 

4.  The  power  to  call  to  mind  objects  named. 

This  will  test  the  integrity  of  the  auditory  speech  area  and  of 
the  association-tracts  between  other  sensory  areas  and  the  tem- 
poral convolutions. 

5.  The  power  to  understand  printed  or  written  words. 

6.  The  power  to  read  aloud  and  to  understand  what  is  read. 

7.  The  power  to  recall  objects  whose  names  are  seen. 

8.  The  power  to  write  spontaneously,  and  to  write  the  names 
of  objects  seen,  heard,  etc. 

9    The  power  to  copy  and  to  write  at  dictation. 
10.  The  power  to  read  understandingly  what  has  been  writ- 
ten. 

These  tests  will  determine  the  condition  of  the  visual  word- 


DISEASES   OF  THE   NERVOUS   SYSTEM.  47 

memories  in  the  angular  gyrus,  and  of  the  connections  between 
this  area  and  surrounding  sensory  and  motor  areas. 

11.  The  power  to  speak  voluntarily,  and  if  it  is  lost,  the  char- 
acter of  its  defects. 

12.  The  power  of  repeating  words  after  another. 

This  will  test  the  integrity  of  Broca's  centre  and  its  associa- 
tion-tracts. 

1.  Word  Deafness. — If  the  memory  of  the  sound  of  the  word  is 
lost,  the  word  cannot  be  called  to  mind  and  cannot  be  recognized 
when  heard.    Show  the  patient  a  watch,  and  he  is  unable  to  name 
it  ;  tell  him  it  is  a  stone,  a  match,  a   watch,  and  notice  whether 
he  dissents  from  the  former  and  gives  signs  of  satisfaction  at  the 
last.     If  he  does,  he  has  only  auditory  amnesia,  but  not  word- 
deafness.     If  not,  he  is  word-deaf,  and  is  unable  to  understand 
what  is  said  to  him.     The  lesion  lies  in  the  posterior  half  of  the 
first  and  second  temporal  convolution  in  the  left  hemisphere  in 
right-handed  ;  in  the  right,  in  left-handed  persons.     This  is  one 
variety  of  aphasia  whose  lesion  is  well  known,  though  it  rarely 
occurs  alone. 

2.  Word  Blindness. — If  the  memory  of  the  appearance  of  the 
word  is  lost,  the  visual  image  of  it  cannot  be  called  to  mind  or 
recognized,  and  then  the  patient  will  be  unable  to  write  spon- 
taneously, for  he  cannot  remember  how  the  letter  looks  which 
he  wishes  to  write  ;  and  he  will  be  unable  to  read  because  the 
shapes  of  the  letters  and  words  seen  arouse  no  recollection.    As  a 
matter  of  fact,  words  are  forgotten   more  easily  than  letters,  and 
if  a  patient  is  to  relearn  to  read  he  must  begin  with  letters  and 
go  on  to  words.    Figures  are  sometimes  recalled  when  words  are 
forgotten,  and  many  a  patient  can  do  mathematical  calculations 
on  paper  who  cannot  read  or  write  ordinary  words.     The  reverse 
may  also  be  true,  the  patient  being  able  to  read  and  write,  but 
being  unable  to  understand  figures  or  calculate.     Such  patients 
may  also  play  cards  or  other  games,  if  they  are  not   psychically 
blind.     It  is  not  infrequently  the  case  that  persons  who  are  thus 
word-blind  can  write  at  dictation,  or  copy,  and  yet  show  no  evi- 
dence of  understanding  what  has  just  been  read  or  written.     A 
distinction  must  be  made  between  those  who  can  and  cannot  do 
these  things,  though  its  pathological  basis  is  still  obscure.     The 
condition  of  visual  amnesia  with  word  blindness  is  due  to  a  lesion 
involving  the  inferior  parietal  convolutions  and  angular  gyrus,  and 
is  often  associated  with  psychical  blindness,  but  may  occur  inde- 


48  DISEASES   OF  THE   NERVOUS   SYSTEM. 

pendently  of  it.  Word-deafness  and  word- blindness  frequently 
occur  together,  and  then  the  lesion  is  found  involving  both  the 
temporal  and  the  angular  convolutions.  Some  cases  of  this  con- 
dition have  depended  on  a  deep  lesion  in  the  temporo-occipital 
region,  breaking  the  association  tracts. 

3.  Motor  Aphasia. — If  the  memory  of  the  effort  needed  to  pro 
nounce  a  word  is  lost,  a  true  paralysis  of  active  speech  occurs, 
though  the  muscles  may  not  be  weakened.     This  is  the  ordinary 
form  of  motor  aphasia,  due  to  a  lesion  of  Broca's  centre.     It  is 
to  be    noted  that  such  a  loss  of  speech  involves  a  loss  of   the 
power  of  repeating  words  after  another,  as  well  as  of  voluntary 
speech,  and  is  not  accompanied  by  any  inability  to  understand 
spoken  or  written  language.     In  the  uneducated,  as  in  children, 
the  acts  of  talking  and  writing  are  closely  joined,  as  may  be  seen 
by  watching  the  lips,  which  move  in  the  act  of  writing.     But 
among  those  accustomed  to  write  much  these  acts  are  independ 
ent,  and  it  is  probable  that  many  educated  aphasics  may  be  able 
to  answer  questions  in  writing  when   their  efforts  at  speech  fail. 
Reading  aloud  will  also  be  lost  in  motor  aphasia,  for  here,  too, 
the  inability  to  articulate  hampers  the  patient. 

4.  Agraphia. — The  independence  of  the  effort-memory  neces 
sary  for  writing,  and  connected  with  movements  of  the  hand  from 
the  effort-memories  of  speech,  has  been  alluded  to.     When  these 
are  lost  alone  the  condition  is  known  as  agraphia.     In  such  a 
state  the  pen  cannot  be  used.    Copying,  writing  at  dictation,  and 
voluntary  writing  are  all  lost.     It  has  been  noted  already  that 
when  a  word  cannot  be  called  to   mind  it,  of  course,  cannot  be 
written.     But  words  can  often  then  be  written  at  dictation,  if  the 
person  is  one  who  writes  much.     Hence  sensory  agraphia  and 
motor  agraphia  must  be  distinguished  ;  the  former  being  a  part 
of  word-blindness,  the  latter  not  at  all  associated  with  inability 
to  read.    The  lesion  of  motor  agraphia  is  unsettled,  though  a  few 
facts  point  to  the  posterior  part  of  the  second  frontal  convolu- 
tion as  the  probable  seat  of  this  function.     It  is  not  unlikely, 
however,  that  the  more  exact  localization   of  fine  movements  of 
the  thumb  and  fingers  in  the  posterior  central  convolution  by 
Horsley  may  be  followed  by  the  discovery  of  the  writing  centre 
in  this  vicinity. 

5.  Paraphasia. — These  forms  of  aphasia  are  due  to  a  loss  of 
distinct  memory-pictures.  The  several  memory-pictures  which 
are  united  in  the  word  image  may  thus  be  reasonably  regarded 


DISEASES   OF   THE   NERVOUS   SYSTEM.  49 

as  separate  from  one  another  in  their  location  in  the  brain.  But 
since  they  are  joined  together  to  form  the  word-image,  it  follows 
that  the  association-fibres  joining  the  various  areas  are  as  neces- 
sary to  the  use  of  even  a  single  word  as  the  various  areas  with 
their  memories.  It  is  really  by  association  only  that  an  object 
or  a  word  becomes  a  subject  of  thought  or  use.  If  these  associa- 
tions are  broken  the  result  is  a  defect  of  language  characterized 
by  the  misplacement  of  words,  and  the  patient  talks  jargon. 

There  are  many  forms  of  paraphasia  as  there  are  many  asso- 
ciation tracts,  and  it  is  not  yet  possible  to  assign  different  cases 
to  their  lesions.  , 

It  is  evident  that  many  differently  located  lesions  will  pro- 
duce disturbances  of  speech.  When  the  entire  cortex  is  dis- 
eased— as  in  paresis — aphasia  also  appears. 

Defects  in  the  appreciation  and  use  of  music  are  called 
amusia,  and  present  the  same  varieties  as  aphasia. 

THE  FRONTAL  REGION. 

There  appears  to  be  a  certain  relation  between  the  frontal 
lobes  of  the  brain  and  the  higher  forms  of  intellectual  activity, 
the  powers  of  fixing  the  attention  and  of  reasoning  and  of  self- 
control.  But  disease  here  does  not  cause  a  loss  of  any  one  men- 
tal faculty,  and  for  the  higher  powers  of  the  mind  a  general  in- 
tegrity of  the  entire  brain,  not  of  any  one  part,  is  necessary. 
When  it  is  considered  that  every  concept  is  made  up  of  numer- 
ous memory  pictures  joined  together,  each  of  which  has  a  sepa- 
rate location  in  the  brain  cortex,  it  becomes  evident  that  to  the 
process  of  thought  a  healthy  state  of  the  entire  cortex  is  neces- 
sary and  also  of  the  white  matter  beneath  it,  through  which  the 
associating  fibres  pass.  And  it  is  therefore  impossible  for  a 
single  lesion  anywhere  to  cause  a  loss  of  memory  or  of  imagina- 
tion or  of  judgment.  Yet  for  the  co-ordination  of  facts  into  or- 
derly series,  for  comparison,  and  for  analysis  of  knowledge 
gained  through  the  senses,  the  healthy  state  of  the  frontal  lobes 
appears  to  be  necessary.  And  lesions  in  the  frontal  region, 
especially  upon  the 'left  side,  are  quite  uniformly  attended  by 
mental  dulness,  apathy,  lack  of  power  of  concentration,  and  im- 
perfect self-control. 

There  are  large  areas  of  the  cortex  of  the  brain  whose  func- 
tion is  undetermined.  These  are  much  more  extensive  on  the 


5<D  DISEASES   OF  THE   NERVOUS   SYSTEM. 

right  hemisphere  than  on  the  left.  There  are  no  definite  symp- 
toms produced,  so  far  as  we  now  know,  by  lesions  in  these  areas  ; 
but  the  negative  fact  is  certain,  that  lesions  in  them  do  not  cause 
disturbances  of  motion,  of  sensation,  or  of  speech. 

The  cortex  of  the  hemispheres  upon  the  base  of  the  brain 
lying  on  the  orbital  plate,  on  the  sphenoid  and  temporal  bones, 
and  on  the  tentorium  cerebelli,  has  as  yet  no  assignable  functions, 
and  lesions  in  these  regions  do  not  produce  recognizable  symp- 
toms. 

SYMPTOMS  OF  CORTICAL  DISEASE. 

In  the  study  of  cases  of  cortical  disease,  it  is  necessary  at  the 
outset  to  distinguish  general  from  local  symptoms,  for  it  is  the 
latter  only  which  enable  one  to  locate  the  lesion.  General  Symp- 
toms are  those  which  are  common  to  various  kinds  of  brain  dis- 
ease in  whatever  region  they  are  located.  They  are  headache, 
vertigo,  digestive  disturbances,  general  convulsions,  optic  neu- 
ritis, with  or  without  blindness,  delirium,  and  coma.  These  are 
due  either  to  an  increase  of  the  intra-cranial  contents  (as  by  the 
growth  of  a  tumor)  and  consequent  pressure,  or  to  some  other 
interference  with  the  normal  condition  in  the  brain.  They  give 
no  evidence  as  to  the  exact  region  of  the  brain  which  is  affected. 
They  merely  indicate  that  the  brain  is  diseased. 

Local  Symptoms,  on  the  other  hand,  depend  entirely  for  their 
production  upon  the  region  of  the  cortex  which  is  invaded. 
They  are  disturbances  of  motion  and  of  sensation  of  various 
kinds,  and  of  sensory  perception  ;  disturbances  of  memory  ;  and 
loss  of  speech.  They  may  be  divided  into  symptoms  of  irrita- 
tion and  symptoms  of  destruction  ;  and  it  is  not  infrequently  the 
case  that  the  former  precede  the  latter  in  the  course  of  a  disease. 
An  irritative  lesion  produces  symptoms  due  to  an  increased  ac- 
tivity of  the  area  affected  ;  e.g.,  spasms,  pain,  tingling  and  numb- 
ness, flashes  of  light,  sounds,  or  hallucinations  of  smell  and  taste. 
A  destructive  lesion  produces  symptoms  due  to  a  loss  of  func- 
tion in  the  area  involved  ;  e.g.,  paralysis,  anaesthesia,  blindness, 
deafness,  loss  of  smell  and  taste,  and  of  the  use  of  language. 
Each  of  these  points  to  a  different  location  of  the  disease  ;  and 
is  essential  to  its  localization. 


DISEASES   OF   THE   NERVOUS    SYSTEM.  51 

II.  TRACTS  WITHIN  THE  BRAIN. 
THE  ASSOCIATION  TRACTS. 

The  first  system  of  fibres  in  the  centrum  ovale  is  the  associa- 
tion system. 

It  can  be  shown  by  careful  dissection  that  each  convolution 
is  joined  to  the  two  adjacent  convolutions  by  fibres  winch  pass 
around  the  separating  fissures.  Also,  that  bundles  of  fibres  exist 
which  pass  from  each  convolution  to  the  convolution  next  but 
one,  and  so  on.  Hence,  it  may  be  stated  that  each  convolution 
has  a  possible  connection  with  every  other.  Besides  this  associ- 
ation of  convolutions  by  small  bundles  of  fibres,  it  is  possible  to 
find  a  distinct  set  of  association  tracts  which  pass  between  more 
or  less  distant  regions.  One  sucli  tract  passes  from  the  frontal 
lobe,  collecting  its  bundles  from  all  three  convolutions,  backward 
to  the  occipital  lobe.  Another  tract  joins  the  occipital  with  the 
anterior  part  of  the  temporal  lobe.  Another  passes  from  the 
upper  two  temporal  convolutions  forward  to  the  third  frontal 
convolution,  passing  beneath  the  island  of  Reil.  And  a  tract 
from  the  frontal  to  the  posterior  temporal  area  may  also  be 
found. 

The  function  of  these  association  fibres  is  to  form  the  physical 
basis  for  the  association  of  concrete  memories  and  of  psychical 
acts,  and  their  integrity  is  necessary  to  thought.  By  studying 
subjectively  the  association  of  ideas  in  the  mind  the  importance 
of  their  function  is  evident.  When  they  are  destroyed  by  dis- 
ease various  forms  of  paraphasia  appear. 

THE   COMMISSURAL  TRACTS. 

The  second  system  of  fibres  in  the  centrum  ovale  is  the  com- 
missural  system.  This  joins  corresponding  areas  of  the  two  hemi- 
spheres with  one  another.  The  comrnissural  fibres  between  the 
frontal,  parietal,  and  occipital  lobes  of  the  two  sides  pass  in  the 
corpus  callosum.  Those  from  the  temporal  lobes  pass  in  the 
anterior  commissure.  The  function  of  these  fibres  is  to  harmo- 
nize the  action  of  the  two  hemispheres.  Simultaneous  movements 
of  like  nature  can  be  made  with  great  facility  with  both  upper 
extremities.  Movements  which  are  difficult  when  attempted  with 
the  left  hand  alone  become  easy  when  associated  with  corre- 


52  DISEASES   OF  THE   NERVOUS   SYSTEM. 

spending  movements  of  the  right  hand— as,  for  example,  drawing 
a  circle,  writing  one's  name.  It  is  the  commissural  fibres  joining 
the  motor  convolutions  only  which  can  be  thus  tested.  Failure 
to  perform  easily  corresponding  bilateral  motions  in  face,  hands, 
or  feet  would  indicate  some  obstruction  to  conduction  in  them. 

THE  PROJECTION   FIBRES. 

The  projection  system  includes  those  fibres  which  join  a  def- 
inite area  of  the  cortex  with  parts  of  the  nervous  system  lying 
below  it,  viz.,  some  nervous  mechanism  in  the  basal  ganglia,  brain 
axis,  or  spinal  cord.  Indirectly,  through  the  medium  of  such 
mechanisms,  the  external  world  is  projected  upon  the  brain  and 
reaches  consciousness,  and  voluntary  impulses  originating  in  the 
brain  are  sent  to  the  muscles.  These  fibres  gather  together  with- 
in the  hemisphere  at  the  upper  level  of  the  basal  ganglia,  and 
either  end  in  the  optic  thalamus,  or  go  on  between  these  ganglia 
through  the  internal  capsule  to  the  brain  axis  and  spinal  cord. 

The  majority  of  these  fibres  end  in  the  optic  thalamus,  which 
is  thus  connected  with  all  parts  of  the  cortex  of  the  brain.  Of 
the  function  of  these  we  know  very  little.  Two  large  bundles, 
however,  are  separable  from  the  mass. 

The  Visual  Tract. — One  of  these  passes  inward  and  forward 
from  the  occipital  lobe,  and  joins  the  pulvinar  of  the  thalamus 
and  the  external  geniculate  body.  This  is  the  visual  tract. 

The  optic  nerves  decussate  partially  at  the  chiasm,  so  that 
each  optic  tract  contains  fibres  from  both  retinae.  Each  tract 
passes  to  the  optic  thalamus,  external  geniculate  body,  and  an- 
terior corpus  quadrigeminum.  Thence  the  fibres  of  the  visual 
tract  pass  out,  to  turn  backward  through  the  internal  capsule  and 
through  the  centrum  ovale  to  the  cortex  of  the  occipital  lobe.  A 
lesion  anywhere  in  this  course  causes  homonyrnous  hemianopsia. 

The  Auditory  Tract. — A  second  bundle  passes  from  the  temporal 
lobe  upward  to  the  thalamus,  internal  geniculate  body,  and  pos- 
terior corpus  quadrigeminum,  in  which  the  auditory  tract  from 
the  acoustic  nucleus  ends.  This  conveys  impulses  of  sound  from 
both  ears  to  each  temporal  lobe,  and  is  the  auditory  tract.  These 
are  the  only  bundles  of  the  thalamic  radiations  whose  function  is 
determined. 

Some  of  the  projection  fibres  pass  on  through  the  internal 
capsule  without  communicating  with  the  basal  ganglia,  and  of 
these  we  know  three  distinct  bundles. 


DISEASES   OF   THE   NERVOUS   SYSTEM.  53 

The  first  is  collected  from  the  three  convolutions  of  the  fron- 
tal lobe,  and  passing  between  the  caudate  and  lenticular  nuclei 
in  the  anterior  division  of  the  internal  capsule,  descends  in  it  to 
the  base  of  the  brain,  and  issuing  in  the  inner  third  of  the  foot  of 
the  crus  cerebri,  passes  down  to  the  pons,  where  it  terminates  in 
nuclei  lying  in  the  ventral  half.  The  nuclei  thus  readied  by 
these  fibres  are  also  joined  by  other  fibres  from  both  hemispheres 
of  the  cerebellum,  which  enter  the  pons  at  its  lateral  surfaces  in 
the  middle  peduncles.  Thus  it  is  evident  that  a  connection  ex- 
ists between  each  frontal  lobe  and  both  cerebellar  hemispheres, 
the  crossed  connection  being  greater  than  the  direct  one.  Of  the 
function  of  this  tract  we  know  nothing. 

The  Motor  Tract. — The  second  bundle  of  the  projection  system 
is  the  motor  tract.  It  comes  from  the  posterior  part  of  the  third 
frontal  convolution,  the  two  central  convolutions,  and  from  the 
para-central  lobule,  and  passes  out  of  the  base  through  the  mid- 
dle third  of  the  crus  cerebri.  Its  fibres  collect  at  the  middle  por- 
tion of  the  upper  surface  of  the  internal  capsule,  those  from  the 
lower  parts  of  the  cortex  passing  straight  inward,  those  from  the 
upper  parts  curving  outward  and  downward  to  pass  around  the 
side  of  the  lateral  ventricle.  Thus  within  the  centrum  ovale, 
these  fibres,  if  looked  at  from  in  front,  appear  like  the  sticks  of 
a  fan,  and  like  those  sticks  their  relative  position  is  altered  in  the 
point  of  junction,  where  those  passing  inward  from  the  lowest 
part  of  the  cortex  lie  in  front  of  those  which  pass  downward 
from  its  upper  part.  Thus  in  the  capsule  the  order  from  before 
backward  is,  first,  the  fibres  conveying  speech  impulses  to  the 
pons  and  medulla  ;  second,  the  fibres  conveying  facial  motor  im- 
pulses to  the  pons  ;  third,  the  fibres  destined  to  the  arm  centres 
of  the  cord  ;  fourth,  the  fibres  transmitting  impulses  to  the  leg 
centres  in  the  cord.  The  fibres  conveying  impulses  to  the  mus- 
cles of  the  trunk  probably  lie  behind  those  to  the  leg. 

From  the  anterior  half  of  the  posterior  division  of  the  capsule 
this  tract  passes  through  the  middle  third  of  each  crus,  through 
the  pons  (where  the  division  to  the  facial  nucleus  crosses  to  the 
opposite  side  and  ends),  and  thence  by  way  of  the  pyramids  of  the 
medulla  to  the  crossed  pyramidal  and  direct  anterior  median 
columns  of  the  spinal  cord.  It  is  evident,  however,  that  the  con- 
centration of  this  tract  is  much  greater  in  the  capsule  than  in  the 
centrum  ovale,  where  the  individual  fibres  are  scattered  among  the 
other  systems  and  occupy  but  a  small  area  from  before  backward. 


54  DISEASES   OF   THE   NERVOUS   SYSTEM. 

Lesions  beneath  the  third  frontal  convolution  of  the  left  side 
produce  motor  aphasia.  Lesions  beneath  the  central  convolu- 
tions in  the  centrum  ovale  produce  paralysis,  which  will  vary  ac- 
cording to  the  position  of  the  lesion.  The  nearer  the  lesion  lies 
to  the  cortex  the  more  will  the  symptoms  resemble  those  of  cor- 
tical disease,  monoplegia  being  the  rule.  The  nearer  the  lesion 
to  the  point  of  junction  at  the  capsule  the  more  will  the  symp- 
toms resemble  those  of  capsule  lesion,  hemiplegia  being  the  rule. 
When  the  motor  tract  is  injured  by  a  lesion  in  the  lower  half  of 
the  pons,  the  result  is  paralysis  of  the  face  on  the  side  of  the 
lesion  and  of  the  arm  and  leg  on  the  opposite  side  (alternating 
paralysis). 

The  Sensory  Tracts. — The  third  set  of  fibres  of  the  projection 
system  includes  those  which  lie  just  posterior  to  the  motor  tract, 
and  which  pass  inward  from  the  parietal  convolutions.  These 
take  a  similar  course  to  those  of  the  motor  tract,  and  fill  up 
to  a  considerable  extent  the  space  between  it  and  the  radia- 
tion of  the  visual  tract,  toward  the  occipital  lobe.  They  are 
mingled  with  fibres  which  pass  to  the  optic  thalamus,  but  are 
separable  from  them  in  foetal  brains,  and  may  be  traced  down 
through  the  capsule  to  the  tegmentum  of  the  crus,  where  they 
divide  into  a  portion  going  to  the  lemniscus,  and  a  portion  going 
to  the  formatio  reticularis.  The  fibres  can  be  traced  through 
these  tracts  downward  to  the  medulla  and  through  the  senso- 
ry decussation  to  the  posterior  pyramids  of  the  medulla  in 
which  the  posterior  columns  of  the  spinal  cord  begin.  This  set 
of  fibres  conveys  the  sensations  of  touch,  pain,  temperature,  and 
muscular  sense,  and  lesions  in  its  course  will  cause  disturbance  of 
these  sensations.  Like  lesions  in  the  motor  tract,  the  rule  ob- 
tains that  the  nearer  the  cortex  the  more  likely  is  the  lesion  to 
cause  an  affection  of  a  single  limb,  while  the  nearer  the  capsule 
the  more  likely  is  the  symptom  produced  to  be  hemianaesthesia. 
A  lesion  in  the  lower  half  of  the  pons  may  produce  alternating 
hemianaesthesia,  the  face  being  anaesthetic  on  the  side  of  the 
lesion,  and  the  limbs  on  the  opposite  side. 

From  these  facts  it  is  evident  that  a  lesion  which  lies  in  the 
centrum  ovale,  at  any  point  posterior  to  the  praecentral  fissure  of 
the  frontal  lobe,  may  produce  recognizable  symptoms,  for  it 
must  affect  either  the  motor,  or  the  sensory,  or  the  visual,  or  the 
auditory  tracts,  or  individual  fibres  of  those  tracts. 


DISEASES    OF   THE   NERVOUS    SYSTEM.  55 


III.  THE  BASAL  GANGLIA. 

The  symptoms  produced  by  lesions  in  the  basal  ganglia — 
corpora  striata  and  optic  thalamus — are  not  to  be  distinguished 
from  those  caused  by  lesions  of  the  projection  tracts  which  lie 
near  them. 

Lesions  of  the  corpora  quadrigemina  cause  nystagmus,  blind- 
ness, and  ophthalmoplegia  (see  page  15). 

IV.  THE  CEREBELLUM. 

The  cerebellum  is  the  central  organ  of  equilibrium.  It  is 
joined  to  the  spinal  cord  by  the  direct  cerebellar  column,  which 
carries  sensory  impulses  up  to  it  through  the  inferior  peduncle. 
It  is  joined  to  the  motor  tract  by  the  middle  peduncle,  which  con- 
veys impulses  to  the  pons  and  thence  to  the  spinal  cord,  directing 
balancing  motions.  It  is  joined  to  the  cerebral  hemispheres  both 
by  the  middle  and  superior  peduncles,  whose  exact  funtions  are 
unknown. 

Lesions  of  the  cerebellum,  or  of  its  peduncles,  cause  staggering 
gait.  This  differs  from  that  in  locomotor  ataxia,  for  there  is  no 
ataxia  of  the  limbs  when  the  patient  lies  down,  giving  support 
to  the  body.  When  the  middle  peduncle  is  irritated  the  patient 
staggers  toward  the  lesion  ;  when  it  is  destroyed  he  staggers 
away  from  the  lesion.  Lesions  of  the  cerebellum  also  produce 
vertigo. 


DISEASES   OF   THE   NERVOUS   SYSTEM.  $? 


THE  CEREBRAL  DISEASES  OF  VASCULAR  ORIGIN. 

The  most  common  cerebral  diseases  are  those  due  to  a  rupt- 
ure of  a  vessel  in  the  brain,  cerebral  hemorrhage,  or  to  a  stoppage 
in  a  cerebral  vessel,  cerebral  embolism  and  cerebral  thrombosis. 

The  cerebral  circulation.     See  "Quain's  Anatomy." 

Pathology. — The  condition  which  leads  to  such  diseases  is 
chronic  endarteritis ;  a  chronic  inflammatory  process  in  the  in- 
tima  and  muscular  coats  of  the  vessels  with  a  production  of 
new  cellular  tissue  which  may  (i)  go  on  until  it  obliterates  the 
lumen  of  the  vessel,  producing  thrombosis,  or  (2)  undergo  calca- 
reous degeneration  roughening  the  wall  and  inducing  fibrin 
deposits,  which  may  occlude  the  vessel,  producing  thrombosis, 
or  be  washed  onward  producing  embolism  ;  or  (3)  undergo 
fatty  degeneration,  thus  eroding  the  intima  and  weakening  the 
muscular  coat  causing  aneurisms  (miliary  or  larger)  which  rupt- 
ure producing  cerebral  hemorrhage.  See  Delafield  and  Prud- 
den's  "  Pathology." 

Pathology  of  Cerebral  Hemorrhage. — The  vessel  ruptures.  The 
blood  spreads  out  in  the  membranes  filling  the  fissures  and  de- 
pressing the  cortex,  or  if  the  hemorrhage  is  subcortical,  tears 
the  surrounding  brain.  A  clot  forms,  thin  and  flat  on  the  cortex? 
globular  in  the  brain,  which  compresses  the  brain-tissue  around 
it.  This  clot  gradually  shrinks,  and  undergoes  absorption  leav- 
ing a  hematin  stain  ;  the  disintegrated  brain-tissue  undergoes 
fatty  degeneration  and  absorption.  There  remains  a  mass  of 
softened  tissue  without  or  with  a  connective-tissue  wall,  or  finally 
a  cyst,  or  a  mass  of  sclerotic  tissue  or  merely  a  scar.  The  torn 
brain  never  reunites.  From  the  point  of  laceration  degeneration 
begins  which  extends  along  the  various  tracts,  e.g.,  descending 
degeneration  in  motor  tract  through  the  cerebral  axis  and  spinal 
cord,  or  ascending  degeneration  in  sensory  tracts  to  the  cortex. 
When  the  pressure  is  removed  the  cortex  may  resume  its  func- 
tion or  the  uninjured  tracts  may  resume  their  function.  Hence 
partial  recovery  is  the  rule  after  cerebral  hemorrhage. 

Pathology  of  Cerebral  Embolism  or  Thrombosis. — The  vessel 
being  occluded  the  brain-tissue  which  is  supplied  with  blood 
through  it  is  cut  off  from  its  nutrition.  The  first  arrest  of  blood 

O 

supply  is  extensive,  but  when  collateral  circulation  is  established 
the  final  area  or  region  which   softens  may  be  small.     In  the 


58  DISEASES   OF   THE   NERVOUS   SYSTEM. 

cortex  the  collateral  supply  by  anastomosing  vessels  is  extensive. 
In  the  basal  ganglia  and  capsule  it  is  very  imperfect.  Hence 
the  permanent  effect  of  occlusion  is  more  serious  in  the  arteries 
entering  the  base  than  in  small  branches  in  the  cortex.  If  large 
vessels  in  the  cortex,  e.g.,  a  main  branch  of  a  Sylvian  artery,  is 
plugged,  the  area  of  softening  may  be  extensive.  A  fatty  de- 
generation and  a  necrosis  of  brain-tissue  follows  the  occlusion  of 
the  vessel.  In  the  softened  tissue  there  are  at  first  extravasations 
of  venous  blood  (red  softening)  ;  later  these  are  absorbed  and 
the  tissue  in  a  stage  of  fatty  degeneration  is  yellow  (yellow  soften- 
ing). If  there  is  simple  necrosis  without  extravasation  or  fatty 
degeneration  the  brain  has  its  natural  color  but  is  soft  (white 
softening).  The  softened  tissue  contracts  leaving  a  depression 
or  a  cavity,  or  a  scar;  in  some  cases  a  cyst  with  smooth  walls 
and  serous  contents. 

The  Situation  of  the  Lesion. — Cerebral  Hemorrhage  :  in  basal 
ganglia  involving  the  internal  capsule  in  fifty  per  cent.,  next  in 
frequency  in  centrum  ovale,  cortex,  pons,  and  ventricles  ;  very 
rarely  in  cerebellum. 

Cerebral  embolism,  forty-nine  per  cent,  left ;  forty-one  per 
cent,  right ;  ten  per  cent,  both  hemispheres.  Central  ganglia 
and  capsule,  sixty  per  cent.  ;  next  in  frequency  cortex  supplied 
by  middle  cerebral  artery,  (i)  motor  area,  (2)  aphasic  area, 
(3)  visual  area.  Least  frequent  pons  and  anterior  or  posterior 
cerebral  arteries. 

Cerebral  thrombosis  in  middle  cerebral,  basilar,  vertebral 
and  anterior  and  posterior  cerebral  vessels  in  order  of  frequency 
named. 

Etiology. — Thrombosis  is  common  below  age  of  forty-five; 
hemorrhage  after  forty-five  ;  age  of  maximum  liability  to  hemor- 
rhage, seventy  to  eighty.  Males  more  liable  than  females  to 
hemorrhage.  Predisposing  causes  of  endarteritis  are  gout, 
lithaemia,  alcoholism,  and  syphilis  ;  associated  diseases  are  ne- 
phritis, endocarditis,  and  emphysema.  Anything  which  increases 
the  heart  action  may  cause  cerebral  hemorrhage,  e.g.,  fright, 
anger,  exertion,  cold  bath.  Anything  which  weakens  its  action 
may  cause  thrombosis. 

Symptoms. — Preliminary  :  For  months  before  the  onset,  ver- 
tigo, insomnia,  headache,  inattention,  and  imperfect  memory. 
Temporary  attacks  of  numbness  in  one-half  of  the  body. 

Sudden  onset,  "apoplexy,"  loss  of  consciousness.     The  result 


DISEASES   OF   THE   NERVOUS   SYSTEM.  59 

depends  on  the  size  and  rapidity  of  hemorrhage,  or  on  the  size  of 
the  vessel  occluded. 

Paralysis  of  one  half  of  the  body  (hemiplegia),  with  coma  and 
convulsions,  is  the  ordinary  form.  Face,  red  ;  pulse,  slow, 
high  tension,  full  ;  respiration,  deep,  stertorous.  Temperature, 
normal,  but  after  some  hours,  high,  102°  to  104°  F.  Deviation  of 
eyes  and  head  may  occur  in  large  lesions  ;  the  patient  looks  to- 
ward the  side  of  lesion.  Pupils  vary.  Inequality  is  most  impor- 
tant symptom,  usually  dilated  on  side  of  lesion.  Hemiplegia, 
hemianaesthesia,  and  hemianopsia,  at  first.  Reflexes,  suspended  ; 
inhibited  by  irritation  for  a  short  time,  then  exaggerated  perma- 
nently. Rigidity  of  limbs  when  hemorrhage  is  large  or  into  the 
ventricle  ;  convulsion  when  hemorrhage  is  on  cortex  or  in  ven- 
tricle. Urine  retained  ;  contains  albumin  and  sugar,  or  may  be 
passed  involuntarily. 

Death  may  occur  in  one  or  two  days,  in  coma,  with  tempera- 
ture of  108°  F. 

Usually  there  is  a  slow  recovery  of  consciousness  and  perma- 
nent paralysis,  which  gradually  decreases  during  a  year,  and  then 
remains  stationary. 

In  lighter  cases  there  may  be  no  loss  of  consciousness,  but 
partial  hemiplegia. 

The  permanent  symptoms  a  week  after  the  acute  onset,  indi- 
cate the  situation  of  the  lesion.  The  symptoms  which  remain  at 
the  end  of  a  month  indicate  its  extent;  e.g.,  hemiplegia  with 
hemianaesthesia  and  hemianopsia  at  first ;  and  permanent  paraly- 
sis, not  total,  in  arm  and  leg  only,  without  sensory  affection 
finally.  In  some  cases  there  is  a  development  after  two  months 
of  contractures  in  the  paralyzed  limbs.  This  indicates  the  exis- 
tence of  descending  degeneration  in  the  motor  tract. 

Course. — After  the  acute  onset,  in  which  the  patient  is  con- 
fined to  bed  for  two  weeks  to  two  months,  depending  on  the 
severity,  the  improvement  begins  ;  the  chief  symptom  being 
hemiplegia.  The  face  is  flat  on  the  paralyzed  side,  and  is  slight- 
ly drawn  by  the  healthy  muscles  away  from  the  paralyzed  side  so 
that  the  mouth  is  crooked.  The  eye  can  be  closed  (vs.  facial 
palsy),  and  can  be  moved  (vs.  ophthalmoplegia).  The  tongue 
deviates  toward  the  paralyzed  side.  The  finer  motions  of  the 
hand  and  arm  are  more  permanently  affected  than  elbow  or 
shoulder  motions;  and  the  upper  extremity  is  carried  in  a  flexed 
position.  The  leg  is  stiff  and  extended,  does  not  bend  easily  at 


60  DISEASES   OF   THE   NERVOUS   SYSTEM. 

the  knee,  and  the  foot  is  dragged  on  its  inner  edge  and  swung 
around  in  walking.  The  muscles  of  the  trunk  and  respiration 
are  very  rarely  affected.  The  bladder  and  rectum  may  not  be 
under  full  control.  There  may  be  a  diminution  of  sensation  in 
the  paralyzed  side,  and  possibly  hemianopsia.  Hemianaesthesia 
or  hemianopsia  may  remain  without  hemiplegia.  A  total  loss  of 
all  senses,  smell,  taste,  sight,  hearing,  and  touch  on  one  side  only, 
occurs  in  hysteria  only.  The  tendon  reflexes  are  usually  much  in- 
creased on  the  paralyzed  side,  and  are  somewhat  increased  on  the 
other  side  as  well.  The  contractures  which  develop  may  cause 
pain,  because  the  limbs  are  rigid.  Otherwise  there  is  no  pain. 

Aphasia  of  some  kind  often  accompanies  right  hemiplegia,  or 
or  may  occur  alone.  (See  p.  47.) 

Some  mental  symptoms  are  usually  observed  after  an  apo- 
plexy, and  may  be  the  only  permanent  symptoms.  There  may 
be  a  lack  of  control  of  the  emotions,  so  that  the  patient  laughs  or 
cries  with  little  cause  ;  an  irritability  of  temper  ;  a  lack  of  judg- 
ment ;  imperfect  memory  of  recent  events  ;  imperfect  power  of 
concentrated  attention  ;  general  bewilderment,  so  that  the  patient 
does  not  recognize  his  surroundings  or  friends  ;  mild  delirium  or 
delusions  ;  or  even  dementia.  These  usually  pass  away  gradu- 
ally, but  sometimes  remain. 

The' various  symptoms,  motor,  sensory,  aphasic,  or  mental,  de- 
pend on  the  situation  of  the  lesion,  and  enable  a  conclusion  to 
be  arrived  at  regarding  it. 

In  any  case  epileptiform  attacks  may  develop,  and  continue 
at  long  intervals  after  an  apoplexy. 

Diagnosis. — Cerebral  Hemorrhage. — In  old  persons  with  athero- 
matous  arteries  and  hypertrophied  heart.  Sudden  onset  of  coma 
during  exertion  or  in  excitement.  Coma  deepens  ;  temperature 
falls  to  97°  to  95°  F.  in  an  hour  ;  after  three  hours  rises  to  101° 
F.  Gradual  recovery  of  consciousness  in  three  to  five  days,  with 
permanent  symptoms  of  hemiplegia. 

Cerebral  Embolism. — At  any  age  with  heart  disease,  or  after 
child-birth.  Sudden  onset  with  no  loss  of  consciousness  or  slight 
condition  of  mental  confusion,  or  rapid  return  of  consciousness. 
Temperature  does  not  fall,  but  may  rise  to  102°  F.  Improve- 
ment occurs  within  twenty-four  hours  to  a  marked  degree,  but 
symptoms  return  in  three  or  four  days  and  are  permanent,  either 
monoplegia,  or  hemiplegia,  or  aphasia.  Jacksonian  epilepsy  may 
develop  after  a  few  months. 


DISEASES   OF   THE   NERVOUS   SYSTEM.  6 1 

Cerebral  Thrombosis. — At  any  age,  but  chiefly  in  syphilitic  per- 
sons and  in  middle-aged  men.  Premonitions  usually  occur. 
Slower  onset  without  coma,  but  dulness  of  mind.  Consciousness 
returns  soon,  if  lost.  Temperature  does  not  fall ;  may  rise  to 
100°  F.  The  paralysis  resembles  that  in  embolism. 

The  diagnosis  between  these  three  conditions  is  never  positive. 

Causes  of  coma  other  than  apoplexy  :  Syncope,  epilepsy, 
uraemia,  diabetes,  alcoholism,  opium  poisoning,  sunstroke,  cere- 
bral injury.  Apopleptic  coma  is  deep  and  patient  cannot  be 
aroused.  Face  is  congested,  eyes  turned  to  one  side,  pupils  un- 
equal, paralysis  is  unilateral,  limbs  may  be  rigid  ;  appearance 
indicates  previous  convulsions.  Physical  examination  reveals 
absence  of  injury  and  presence  of  predisposing  disease,  e.g.,  athe- 
roma,  endarteritis,  cardiac  disease,  albuminuria,  syphilitic  scars. 
The  absence  of  diagnostic  signs  of  other  causes  of  coma  confirms 
the  diagnosis  of  apoplexy.  Reflex  movements  can  be  caused  on 
non-paralyzed  side  by  producing  pain.  The  tendon  reflexes  are 
often  lost  at  the  onset.  The  cremasteric  reflex  is  always  lost  on 
the  paralyzed  side. 

Prognosis  depends  on  the  depth  of  coma,  on  the  condition  of 
pulse  and  respiration,  on  the  constitution  and  age  of  the  patient, 
and  on  the  number  of  previous  attacks. 

Treatment  in  stage  of  apoplexy  :  Rest  ;  quiet  ;  ice-bag  to 
head  ;  venesection  in  plethoric  cases  ;  purgatives  of  a  drastic 
nature  ;  stimulants  if  heart  failure  is  present. 

For  hemiplegia  :  Exercise  ;  massage  ;  faradism  to  the  mus- 
cles for  purpose  of  exercise. 

Medicines  are  of  no  use  in  either  stage. 

CEREBRAL  ATROPHY. 

Cases  of  cerebral  disease  in  children,  either  unilateral  or  bi- 
lateral, present  some  peculiar  features  of  three  different  types. 

First,  cases  of  hemiplegia  with  or  without  athetosis. 

Secondly,  cases  of  mental  defects  of  various  grades. 

Thirdly,  cases  of  sensory  defect  of  different  types.  Epilepti- 
form  seizures  of  petit  mat  or  of  grand  ma/>type  occur  frequently 
in  patients  who  may  be  assigned  to  any  one  of  these  groups. 

I.  Infantile  Hemiplegia.— -The  symptoms  are  the  sudden  de- 
velopment of  a  unilateral  paralysis  after  a  series  of  convul- 
sions attended  by  high  fever  and  its  attendant  discomforts,  and 


62  DISEASES   OF   THE   NERVOUS   SYSTEM. 

a  period  of  unconsciousness  of  varying  duration  ;  then  a  grad- 
ual improvement  in  the  paralysis  after  the  active  manifesta- 
tions of  the  onset  have  subsided  ;  and  finally,  a  stationary  condi- 
tion, in  which  the  face  is  but  slightly  affected  in  its  voluntary  or 
automatic  movements  ;  the  speech  is  usually  regained,  if  it  had 
been  lost ;  the  arm  is  quite  seriously  paralyzed,  the  fingers  being 
stiff  and  awkward,  and  sometimes  being  in  constant  slow  invol- 
untary motion  (athetosis)  ;  the  leg  is  held  rather  rigid,  so  that 
the  child  limps  in  walking,  and  often  develops  a  club-foot. 
There  are,  of  course,  on  the  one  hand,  light  cases  in  which  the 
symptoms  finally  amount  merely  to  clumsiness  in  the  fingers. 
There  are,  on  the  other  hand,  severe  cases  in  which  a  double 
hemiplegia  has  occurred,  both  halves  of  the  body  being  equally 
affected,  and  in  which  both  arms  are  useless  and  both  legs  so 
stiff,  so  closely  adducted,  and  so  helpless  that  walking  is  impos- 
sible (diplegin).  The  latter  are  cases  in  which  all  the  symptoms 
date  from  birth.  In  all  cases  the  paralyzed  limbs  are  found  to  be 
affected  in  their  growth  and  development,  so  that  they  are 
smaller,  colder,  stiffer,  and  weaker  than  the  others  ;  the  reflexes 
are  exaggerated,  but  the  electrical  reactions  are  not  qualitatively 
changed,  and  the  sensation  is  normal.  This  condition  remains 
through  life  as  a  permanent  defect,  and  although  the  division  of 
contractured  muscles  or  tendons,  and  the  application  of  ingen- 
ious apparatus,  may  correct  deformities  and  make  the  paralyzed 
parts  fairly  useful,  and  although  the  application  of  electricity  to 
the  muscles  chiefly  affected  may  increase  their  nutrition  and  thus 
prevent  contracture  which  comes  from  the  unbalanced  strain 
between  the  various  muscles,  yet  any  great  degree  of  improve- 
ment is  impossible.  In  more  than  one-half  of  these  cases  epi- 
leptic attacks  are  of  frequent  occurrence. 

The  cases  which  date  from  birth  must  be  divided  into  those 
in  which  there  has  been  evidence  of  traumatism  during  labor, 
and  those  in  which  there  was  none.  In  the  former  class  it  may 
be  stated  confidently  that  cerebral  hemorrhage,  usually  menin- 
geal,  is  the  cause  of  the  symptoms.  In  the  latter  class  it  is  prob- 
,jible  that  an  intra-uterine  encephalitis  or  some  unknown  cause 
ha?  prevented  the  foetal  brain  from  developing. 

^he  cases  which  have  developed  suddenly  after  birth  are 
cases  in  which  the  ordinary  causes  of  hemiplegia  in  adults  have 
been  a^ng*  a°d  must  be  traced  either  to  encephalitis,  hemor- 
rhage, Pr  embolism,  or  disease  of  the  vessels.  The  degree  of 


\ 


DISEASES   OF   THE   NERVOUS   SYSTEM.  63 

spontaneous  recovery  in  any  case  can  be  pretty  well  determined 
by  an  examination  at  the  end  of  the  second  year.  A  complete 
cure  never  occurs. 

The  fits  in  organic  epilepsy  are  likely  to  be  more  frequent 
and  severe  than  in  idiopathic  epilepsy  ;  as  many  as  twenty  con- 
vulsions may  occur  daily  for  weeks  at  a  time.  These  fits  do 
not  destroy  life,  but  render  life  a  burden.  When,  however,  they 
are  infrequent  they  may  be  benefited  to  some  degree  by  the  use 
of  bromides. 

II.  The  second  class  of  cases  presents  mental   defects   more 
noticeable   than  physical  symptoms.     The  child  may  be  slow  in 
learning  to  talk,  may  seem  unable  to  fix  its  attention  upon  any- 
thing continuously,  may  be  exceedingly  active,  in  constant   mo- 
tion— the  activity  being,   however,   aimless  ;  may  throw    things 
about,  or  tear  things  up,  or  put  everything  into  its  mouth  ;  may 
be  very  difficult  to  manage  because  of  its  inability  to  retain  and 
combine  impressions  with  sufficient  power  to  reason  upon  them  ; 
and  may,  therefore,  be  incapable  of  appreciating  the  meaning  of 
punishment,  if  this  be  inflicted.     Such  children  may  have  good 
powers  of  perception,  may  recognize  persons  and  objects,  show 
pleasure  at  bright  colors,  or  music,  or  caresses,  but   fail  to  show 
evidence  of  thought  in  the  sense  of  reasoning  power,  judgment, 
or  self-control.     Some   patients   constantly  drule  at  the   mouth, 
cannot  be   taught  cleanly  habits,  and   are   manifestly  imbecile. 
Other  patients  are  quite  bright  in  many  directions,  may  even  be 
precocious,  show  talents  in  music,  or  drawing,  or  fondness  for 
mathematics,  designing,  languages  ;  yet  are  apparently  unable  to 
appreciate  moral  ideas,  cannot   be  taught   to  tell   the  truth,  are 
cruel  and  bad,  will  not  control  any  of  their  impulses,  and  so  are 
the  distress  and  despair  of  parents  and  teachers.     It  is  those  men- 
tal qualities  which  are  the  product  of  the  highest  evolution  which 
have  failed  to  develop  in  this  class  of  cases.     The  final  result  is 
that  they  have  to   be  taken  care  of  all  their  lives,  either  at  home 
or  by  attendants,  being  incapable  of  supporting  themselves   or 
directing  their  conduct.     Many  of  them  have  epilepsy.     Some  of 
them  have  hemiplegia. 

III.  The   third  class  of  cases  is   less  common  than  the  two 
preceding,  and  is  likely  to  escape  observation   unless  carefully 
investigated.     The  patients  belonging  to  this  class  may  be  hemi- 
plegic  or  may  present  no  motor  or  mental  defects,  though  they 
may  be  the  subjects  of  epilepsy.     They  do  have  defects  of  sen- 


64  DISEASES   OF   THE   NERVOUS   SYSTEM. 

sory  perception.  Such  defect  may  be  in  the  form  of  hemianopsia 
or  of  deafness.  It  is  probable  that  many  cases  of  deafmutism 
belong  to  this  class,  and  in  some  persons,  as  in  Laura  Bridgeman, 
deafness,  dumbness,  and  blindness  coincide. 

The  pathological  changes  in  the  brain  in  these  various  cases  dif- 
fer widely,  and  are  as  follows,  in  the  order  of  frequency  : 

Porencephalus,  a  localized  atrophy  or  agenesis,  leaving  a  cav- 
ity in  the  cerebral  hemisphere,  which  may  be  deep  enough  to 
open  into  the  ventricle. 

Sclerotic  atrophy,  an  atrophic  condition  of  the  brain  with  an 
increase  of  connective  tissue  and  disappearance  of  the  nervous 
elements  ;  affecting  both  hemispheres,  or  one  only,  or  a  part  of 
one  only  ;  or  limited  to  small  areas  in  various  parts. 

Maldevelopment  and  apparent  atrophic  condition  of  the  minute 
structures  of  the  hemisphere,  chiefly  cortical,  the  cells  resembling 
those  of  a  new-born  child,  but  with  no  apparent  gross  defects  in 
the  brain. 

Atrophy,  consequent  upon  the  condition  of  softening  pro- 
duced by  embolism  or  thrombosis,  and  limited  in  extent  to  cer- 
tain arterial  districts  of  the  brain. 

Meningo-encephalitis,  a  condition  shown  by  thickening  and  ad- 
hesion between  the  pia  and  the  brain,  with  destruction  of  the 
cerebral  cells  and  atrophy  of  the  cortex. 

Cysts  lying  on  the  brain  and  producing  atrophy  by  pressure, 
or  associated  with  atrophy  due  to  the  original  lesion  of  which  the 
cyst  remains  as  a  trace. 

Hemorrhage  on,  or  in,  the  brain,  as  shown  by  the  remains  of  a 
clot,  or  by  hematin  staining  of  a  cyst,  of  the  pia,  or  of  the  scle- 
rotic tissue. 

Hydrocephalus  with  extreme  dilatation  of  the  ventricles,  so  that 
the  brain-tissue  is  reduced  to  a  mere  wall  about  the  cavity. 

These  are  the  conditions  found  at  death  in  cases  presenting 
the  clinical  features  just  studied.  It  is  evident  that  they  have 
this  in  common,  namely,  a  condition  of  atrophy  of  the  brain. 
The  origin  of  this  atrophy  is  not  always  clear.  In  some  cases  it 
is  clearly  congenital  and  due  to  a  maldevelopment  of  the  em- 
bryo. In  other  cases  it  is  clearly  traceable  to  injuries  at  birth. 
In  other  cases  it  must  be  ascribed  to  affections  of  various  kinds, 
such  as  inflammations  of  the  membranes,  or  of  the  brain  sub- 
stance, or  vascular  lesions  and  their  consequences,  such  as  occur 
in  adults.  But  it  is  evident  that  the  various  processes  of  disease 


DISEASES   OF   THE   NERVOUS   SYSTEM.  65 

have  as  a  fairly  uniform  result  a  condition  of  atrophy  with  scle- 
rosis of  the  brain,  which  may  be  termed  sclerotic  atrophy.  The 
difference  in  the  clinical  types  is  due  to  the  varying  situation  of 
the  lesion  rather  than  to  its  varying  nature. 

For  such  conditions  there  can  be  no  treatment. 

TUMORS  OF  THE  BRAIN. 

Varieties  in  order  of  frequency  : 

Gumma  :  soft  gelatinous,  or  hard  cellular,  situated  on  base  or 
in  cortex,  usually  beginning  in  meninges. 

Tubercular:  hard  masses,  often  multiple,  especially  frequent 
in  children,  situated  anywhere,  sometimes  primary,  usually  sec- 
ondary. This  is  the  variety  in  more  than  one-half  the  cases  in 
children. 

Glioma  :  peculiar  to  the  nervous  system,  cells  and  fibres  like 
the  neuroglia,  usually  infiltrated  and  without  boundaries,  but 
single,  usually  vascular,  hence  symptoms  vary  and  hemorrhage 
occurs  ;  usually  situated  in  the  white  substance. 

Sarcoma  of  all  varieties  :  fibro-,  round-cell,  spindle-cell,  glio- 
sarcoma,  begin  from  connective  tissue  of  membranes  as  a  rule, 
sometimes  in  the  brain.  Hard  single  tumors,  of  various  sizes, 
easily  separable  and  well  defined,  situated  on  base,  in  meninges, 
in  cerebellum. 

Carcinoma  :  rare,  usually  secondary. 

Occasional  varieties  are  fibromata,  osteomata,  psammomata, 
cholesteatomata,  angiomata,  lipomata,rechinococcus,  and  cysti- 
cercus. 

Aneurisms  of  the  base  give  rise  to  symptoms  of  tumor. 

For  Pathology  of  Tumors  see  Delafield  and  Prudden's  "  Pathology." 

Causes  of  Brain  Tumor. — i.  Predisposing  :  Sex :  males  twice 
as  frequently  affected  as  females.  Age  :  children  most  liable,  as 
tubercular  tumors  are  frequent.  Young  adults  next.  Old  age  is 
quite  exempt,  except  from  carcinoma. 

2.  Exciting.  Injuries.  Severe  emotional  shock.  Unknown 
in  large  majority. 

Situation. — Cerebral  cortex,  twenty-five  per  cent;  cerebel- 
lum, twenty-five  per  cent.;  centrum  ovale,  fifteen  per  cent.;  basal 
ganglia,  ten  per  cent.;  pons,  ten  per  cent.;  crus  and  corpora 
quadrigemina,  ten  per  cent.  Others  five  per  cent. 


66  DISEASES   OF  THE   NERVOUS   SYSTEM. 

Effects  of  Brain  Tumor. — i.  Direct  effects,  irritation  of  gray 
matter  with  nervous  discharges  ;  and  destruction  of  brain  tissue. 

2.  Indirect  effects.  General  pressure  on  entire  brain.  This 
may  be  limited  by  the  falx  or  tentorium.  It  produces  hydro- 
cephalus  by  pressure  on  ventricle  or  veins  of  Galen.  Vascular 
disturbance  by  pressure  on  arteries  and  veins.  Meningitis,  local- 
ized and  not  purulent  except  in  tubercular  cases.  Thinning  of 
cranial  bones. 

Effects  of  increased  pressure  are  seen  after  death  in  flatten- 
ing of  the  convolutions,  anaemia  and  pallor  of  the  brain,  dry 
sticky  state  of  membranes  and  distention  of  ventricles  by  serum. 

Symptoms  of  Brain  Tumor. — I.  General  symptoms  depend  on 
existence  of  a  new  growth  independent  of  its  position. 

Headache  in  ninety-five  per  cent.,  constant  or  intermittent  : 
general  or  local  ;  dull  and  deep,  increased  by  anything  which 
deranges  the  cerebral  circulation.  Sometimes  head  is  tender 
to  percussion  at  certain  points  :  may  have  evidence  of  pain  even 
in  state  of  stupor  :  it  may  be  agonizing  ;  it  may  give  feeling  of 
band  about  head  :  it  is  often  worse  at  night,  causing  insomnia, 
especially  in  gumma. 

Mental  disturbance,  eighty-five  per  cent.  Dulness  and  apathy, 
with  imperfect  attention  and  memory.  Depression  and  emo- 
tional state.  Slow  speech,  gradual  mental  failure,  childishness1 
and  dementia  ;  fainting  attacks,  stupor  and  coma  in  the  last 
stage.  Occasionally  delirium  and  active  insanity. 

Optic  neuritis,  eighty  per  cent.  Venous  congestion.  Swell- 
ing of  papilla,  loss  of  disc  outline ;  radiating  appearance  about 
the  disc  and  hemorrhages  ;  then  optic  nerve  atrophy  leaving 
white  or  gray  disc.  In  cases  of  subcortical  tumor  of  small  size 
it  may  be  absent.  Sight  may  be  affected  ;  visual  field  small 
and  irregular,  or  unimpaired  for  a  time. 

Vertigo  or  sense  of  giddiness,  frequent  in  tumors  in  posterior 
fossa.  May  occur  in  tumors  anywhere  on  change  of  position. 
May  be  due  to  paralysis  of  one  or  more  ocular  muscles. 

Vomiting,  with  or  without  nausea  or  relation  to  food.  Fre- 
quent in  tumors  in  posterior  fossa. 

General  convulsions  of  epileptic  type.    Petit  mal  vv grand  mal. 

Nystagmus,  lateral  oscillation  of  eyes.  Frequent  in  disease 
of  corpora  quadrigemina  and  cerebellum. 

Loss  of  control  over  sphincters  occurs,  especially  with  tumors 
in  the  frontal  lobes. 


DISEASES   OF   THE   NERVOUS   SYSTEM.  67 

Glycosuria  and  polyurea,  especially  with  tumors  in  the  pos- 
terior fossa. 

Slow  pulse  ;  50  to  60. 

II.  Local  Symptoms  dependent  upon  the  position  of  the 
tumor. 

Frontal  Lobes:  Mental  dulness,  lack  of  control  of  emotions, 
irritability,  inattention,  and  childishness,  dementia,  loss  of  sense 
of  smell. 

Left  third  frontal  convolution.     Motor  aphasia. 

Central  Convolutions,  and  motor  tract.  Monospasm  and  mono- 
plegia  when  in  or  near  cortex.  Hemispasm  and  hemiplegia, 
when  deep  or  in  capsule.  Sometimes  slight  anaesthesia  in  par- 
alyzed part. 

Occipital  Lobe  and  visual  tract.  Hemianopsia,  noticed  by  pa- 
tient as  unilateral  blindness.  Visual  hallucinations  and  flashes 
of  light  on  one  side. 

Left  Temporal  fast  and  second  convolutions.  Sensory  aphasia  : 
form,  word-deafness. 

Left  Lower  Parietal  lobule  and  angular  gyrus  or  in  occipito- 
temporal  tract.  Sensory  aphasia  :  form,  word-blindness. 

Base  of  brain. 

Anterior  fossa  :  Loss  of  smell. 

Middle  fossa:  Hemianopsia,  paralysis  of  ocular  muscles,  III., 
IV.,  VI.;  neuralgia  of  face  and  anaesthesia,  V.;  paralysis  of  III. 
and  opposite  hemiplegia,  neuroparalytic  ophthalmia,  nystagmus  ; 
bilaterial  spastic  paralysis,  deafness. 

Posterior  fossa :  Paralysis  of  VII.,  IX.,  X.,  XL,  XII.;  vertigo 
and  aural  symptoms;  cerebellar  ataxia,  tendency  to  one  side; 
paralysis  wide-spread  from  medulla  disease. 

Cerebellum  :  Vertigo,  vomiting,  cerebellar  ataxia  when  mid- 
dle lobe  is  involved  ;  headache,  frontal  or  occipital  and  severe  ; 
optic  neuritis  early. 

Diagnosis. — Cerebral  symptoms  :  general  alone,  or  general  + 
local,  point  to  the  presence  of  a  tumor. 

Differentiation  from  chronic  nephritis  :  By  examination  of 
urine  ;  by  condition  of  heart,  arteries,  and  blood-pressure  ;  by 
appearance  of  optic  disc  and  retina  in  many  cases,  haemorrhages 
more  frequent  and  white  spots  far  from  disc  ;  by  character  of 
headache,  more  severe  in  tumor  ;  by  age  of  patient,  young  per- 
son =  tumor. 

From    hypermetropia   with    astigmatism    and    anaemia,   with 


68  DISEASES   OF   THE   NERVOUS   SYSTEM. 

menstrual  disorder  :  By  examination  of  eyes  and  relief  of  glasses  ; 
by  cure  of  anaemia  by  diet,  iron,  and  aloes  ;  by  slight  degree  of 
headache  and  neuritis. 

From  hysteria  with  migraine  :  By  study  of  the  patient  and 
separation  of  real  symptoms  ;  by  condition  of  the  optic  disc. 

From  abscess  :  By  history  of  trauma  or  of  otitis  media  ;  by 
severity  of  early  symptoms  in  abscess  ;  by  fever  in  abscess  ;  by 
late  development  of  optic  neuritis,  rare  in  abscess. 

To  determine  the  location  :  Study  carefully  the  local  symp- 
toms, "  signal  symptom,"  e.g.,  numbness  and  twitching  of  thumb. 
Study  also  the  order  of  appearance  of  local  symptoms  :  thumb, 
hand,  face.  Compare  the  several  local  symptoms,  paralysis  + 
aphasia,  or  +  hemianopsia. 

To  determine  the  variety  :  Estimate  probable  frequency  of 
various  tumors  at  different  ages.  Look  for  history  of  syphilis, 
tuberculosis,  cancer,  or  sarcoma.  Study  rapidity  of  onset  ;  gli- 
oma,  tubercle,  cancer  are  rapid.  Study  signs  of  irritation  ;  more 
frequent  in  glioma  and  meningeal  tumors.  Study  signs  of  varia- 
tion in  severity  of  symptoms  ;  more  variation  in  glioma.  Study 
situation  of  the  tumor  ;  basal  tumors  are  often  gum  ma,  tubercle 
sarcoma.  Intra-cerebral  tumors  are  often  glioma,  sarcoma.  Pe- 
culiar forms  of  hemiopia  and  early  optic  neuritis  indicate  sar- 
coma of  pituitary  body  or  aneurism. 

Course  of  the  disease  :  Begins  with  general  symptoms  usually. 
Sometimes  begins  with  local  spasm  or  a  general  convulsion. 
Gradual  increase  in  severity  and  number  of  symptoms.  Finally 
death  in  stupor  or  in  general  convulsion  or  suddenly,  from  heart 
failure,  or  recovery  under  specific  treatment. 

Duration  is  from  one  to  three  years. 

Prognosis  bad  excepting  in  gumma  and  when  tumor  can  be 
removed. 

Treatment. — For  gumma  :   Inunctions   of  mercury  and   KI   to 
three  hundred  grains  daily. 

Surgical  treatment  :  Removal  is  possible  when  diagnosis  of 
location  is  exact.  There  is  danger  of  return. 

For  Cranio-Cerebral  Topography,  see  page  40. 

ABSCESS  IN  THE  BRAIN. 

Acute  encephalitis  with  formation  of  pus  results  in  an  ab- 
scess. The  abscess  may  extend  rapidly,  not  being  encapsulated, 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


69 


and  cause  death  ;  or  it  may  become  encapsulated  and  develop 
slowly,  or  become  stationary  and  remain  for  years  as  a  foreign 
substance  producing  no  symptoms,  but  finally  enlarge  or  break. 
Occasionally  multiple  abscesses  develop  in  the  brain  secondary 
to  pyaemia,  producing  cerebral  symptoms  in  the  course  of  that 
disease.  There  may  be  a  secondary  meningitis  in  either  form. 

Situation. — Is  usually  in  the  temporo-sphenoid  lobe  or  in  the 
frontal  lobe  or  in  the  cerebellum,  in  the  white  matter. 

Causes. — Chronic  otitis  media,  forty  per  cent.  Fracture  of 
cranial  bones,  thirty-five  per  cent.  Chronic  rhinitis,  ten  per 
cent.  Caries  of  any  cranial  bone,  ten  per  cent.  Secondary  to 
infectious  diseases,  five  per  cent. 

Symptoms. — After  an  injury  or  after  otorrhoea  or  other  cause 
cerebral  symptoms  develop  suddenly  ;  severe  headache,  vomit- 
ing, mental  distress  and  dulness,  stupor,  a  chill,  a  high  tempera- 
ture for  a  day  or  two  ;  possibly  convulsions  ;  rarely  local  symp- 
toms ;  hemiplegia,  hemianopsia,  aphasia,  cerebellar  staggering. 
In  a  week  the  patient  is  very  ill,  with  irregular  temperature, 
sometimes  with  chills,  sometimes  no  fever  ;  slow  pulse  ;  intense 
pain,  delirium,  stupor,  and  optic  neuritis.  If  abscess  extends 
death  follows  in  two  weeks,  or  suddenly  from  rupture.  If  ab- 
scess discharges  into  ear  or  nose,  or  if  it  can  be  opened,  symp- 
toms subside.  Rarely  symptoms  subside  spontaneously  slowly, 
the  abscess  becoming  encapsulated  and  latent,  and  patient  ap- 
parently recovers,  but  is  subject  to  headache  and  vertigo  ;  and 
has  a  relapse  later. 


Diagnosis. — 

ABSCESS 

Temperature  normal  or  not  high. 
Pulse  slow. 
Patient  in  stupor. 
Spasms  and  rigidity  rare. 
Cranial  nerves  not  involved. 
Optic  neuritis  frequent. 

ABSCESS 

Temperature  normal  or  not  high. 

Pulse  slow. 

Chill  at  onset  not  repeated. 

Little  sweating. 

Head  tender  to  percussion  ? 


vs.  MENINGITIS. 

Temperature  high  without  remission. 
Pulse  rapid. 

Patient  irritable,  all  senses  over  acute. 
Spasms  and  rigidity  frequent. 
Cranial  nerves  involved  early. 
Optic  neuritis  rare. 

vs.   THROMBOSIS  OF  LATERAL  SINUS. 

Temperature  high  with  remissions. 

Pulse  rapid,  weak. 

Chills  frequently  repeated. 

Profuse  sweating. 

Pain  over  mastoid  and  jugular.      , 

Thrombi  in  lungs. 


7O  DISEASES   OF   THE   NERVOUS   SYSTEM. 

Diagnosis  of  location  is  made  partly  from  the  exciting  cause 
and  partly  from  the  local  symptoms. 

Prognosis  fatal,  unless  abscess  can  be  opened. 

Treatment. — In  the  few  cases  in  which  the  abscess  can  be 
located  operation  of  trephining  and  drainage. 

CEREBRO-SPINAL  SCLEROSIS. 

Multiple  or  disseminated  sclerosis  is  a  rare  disease  affecting 
the  brain  and  spinal  cord  together.  Small  regions  of  sclerotic 
tissue  are  found  irregularly  scattered  through  the  entire  nervous 
system,  without  destruction  of  the  axis  cylinders  of  the  nerve 
tracts.  Its  cause  is  unknown. 

Symptoms. — Headache,  vertigo,  malaise,  mental  irritability, 
inattention,  imperfect  memory,  lack  of  self-control,  and  inability 
to  work.  Later  tremor  of  hands  increased  by  an  effort  to  hold 
them  still,  nystagmus,  increased  knee-jerk,  stiff  spastic  gait, 
weakness,  and  finally  general  tremor  on  effort.  Slow  speech, 
each  syllable  separately  enunciated  without  variation  of  tone. 
Optic  atrophy.  Dementia  and  attacks  of  epilepsy  and  hemi- 
plegia  may  finally  occur. 

Course  is  exceedingly  irregular,  symptoms  may  disappear  for 
months  and  then  return.  The  disease  is  often  mistaken  for 
hysteria. 

Diagnosis  is  made  by  excluding  all  other  organic  diseases,  by 
nystagmus,  tremor,  and  speech. 

Treatment. — Physostigmine,  Jg-  gr.  daily  ;  solanin,  |  gr.  daily, 
increased. 


FUNCTIONAL  NERVOUS  DISEASES. 

NEURASTHENIA. 

Nervous  prostration,  nerve  tire,  nervous  irritable  weakness  is 
a  functional  disease  of  the  entire  nervous  system,  brain,  spinal 
cord,  spinal  and  sympathetic  nerves,  dependent  upon  malnutri- 
tion, characterized  by  nervous  weakness  and  irritability. 

A  balance  between  expenditure  of  energy  and  nutrition  must 
be  preserved. 

Brain  over-work  or  anxiety  ; 

Spinal  cord  over-work  by  long  marches  or  sexual  over-action  ; 

Nerve  over-work  by  various  occupations  in  which  a  single  act 
is  repeated  ; 

Vaso-motor  work  in  maintaining  vascular  tone  and  nutritive 
processes,  all  require  a  sound  basis  and  rest  at  periods. 

When  balance  between  store  and  expenditure  of  energy  is 
broken,  exhaustion  results.  Then  nature  enforces  rest  by  fa- 
tigue, by  sleep.  One  may  disregard  nature,  but  if  so  one  must 
pay  the  penalty. 

Causes. — I.  Excessive  expenditure  of  nerve  energy. 

Primary  neurasthenia  more  common  than  secondary. 

Influences  favoring  its  production  : 

1.  Bad  hereditary  influences.     Weak  nervous  system. 

2.  Feebleness  in  childhood,  with  poor  nervous  system. 

3.  Wrong  methods  of  training  and  education. 

4.  The  struggle  for  existence.     Kant's  rule,  eight  hours  for 

Avork,  eight  hours  for  diversion,  eight  hours  for  sleep. 

5.  Anxiety,  worry,  mental  depression,  fear. 

6.  Mental  or  physical  over-work. 

7.  Sexual  excesses. 

II.  Deficient  supply  of  nervous  energy. 
Secondary  neurasthensia. 
Influences  favoring  its  production. 

i.  Weakening  diseases  of  all  kinds  of  organic  nature. 


72  DISEASES   OF   THE   NERVOUS   SYSTEM. 

2.  Indigestion     and    dyspepsia,    with    auto-infection     by 

products. 

3.  Gout,  rheumatism,  uric-acid  diathesis. 

4.  Infectious  diseases,  typhoid,  grippe,  malaria. 

5.  Alcoholism  or  abuse  of  drugs. 

Result  of  the  action  of  these  causes  is  to  produce  malnutri- 
tion of  the  nervous  system  and  state  of  irritable  weakness. 

1.  The   power  of  continuous  activity  is  impaired  ;  weakness 
results  ;  hence,  mental  work  is  imperfect ;  attention  flags  ;  mem- 
ory fails  ;  ambition  ceases  ;   physical  activity  is  imperfect  ;   ex- 
ercise tires  one  ;  lassitude  ;   vegetative  functions    are    impaired. 
Digestion    is    poor;  constipation    occurs;   vascular   tone    is  im- 
paired ;   heart   feeble.     Balance    must    be    maintained    between 
blood   supply  and  functional   activity.     When   this  is  impaired 
work    is    impossible.     Secretions   are    changed    in    amount    and 
character,  e.g.,  urine. 

2.  The  power  of  mental  and  physical  control  is  impaired  and 
irritability  results  ;  inhibition  may  be  partly  automatic  and  partly 
conscious  ;  it  must  be  conscious  and  voluntary  to  prevent  mor- 
bid fear  and  apprehension  ;  influence  of  fear  is  to  inhibit  all  ner- 
vous acts — e.g.,  walking  on  ice,  oral  examination,  stage  fright ; 
this  control  is  weakened,  and  hence  irritability  results. 

Symptoms  of  Neurasthenia. — 

1.  Cerebral :  Headache — dull,  occipital,  frontal ;  sensitiveness 
of  scalp  ;  vertigo  ;  insomnia  ;  cerebral  sensations — fulness,  band, 
pulsation. 

2.  Mental  :  Apprehension — morbid  fears,  of   places,  people, 
solitude,  etc.;  inattention  and  forgetfulness ;  incapacity  for  work  ; 
idiosyncrasies  become  prominent ;  irritability  of  temper  ensues  ; 
anxiety  and  exhaustion  ;  imperfect  respiration  and  rapid  pulse. 

3.  Spinal  :  Pain,  especially  in  nape  of  neck  and  sacrum  ;  irri- 
tation ;  hypersensitiveness  ;  sensitiveness  about   ribs  and   inter- 
costal nerves  ;  weakness,  legs  give  out ;  sexual  irritation,   erec- 
tions, impaired  power  ;  emissions  ;  bladder  irritability,  frequent 
micturition. 

4.  Vaso-motor  :  Flushes,  cold  extremities  ;  undue  sweating  ; 
transient  blueness  or  oedema ;  tac/ie  cerebrale  of  Trousseau  ;  tachy- 
cardia ;  palpitation. 

5.  Gastro  -  intestinal :  Indigestion    and  dyspepsia,   especially 
acid  stomach  ;  imperfect  liver  action  ;  constipation  ;  pseudomem- 
branous  colitis  ;  distention  of  abdomen  with  gas. 


DISEASES   OF   THE   NERVOUS   SYSTEM.  73 

6.  Sensory  and  motor  symptoms:  Indefinite  pains  and  paraes- 
thesia  ;  joint  affections  ;  apparent  paralysis — no  change  in  elec- 
tric activity  ;  vision  imperfect  ;  asthenopia  ;  visual  field  may  be 
retracted.  Other  senses  rarely  affected;  tinnitus. 

Diagnosis  made  by  the  existence  of  a  cause  ;  the  absence  of 
objective  signs  of  organic  disease  ;  the  temperament  of  the  pa- 
tient ;  the  variability  of  symptoms  ;  the  disproportion  between 
complaint  and  actual  power. 

Treatment. — Absolute  necessity  of  establishing  nerve-energy 
by  restoring  balance  between  store  and  expenditure.  Hence  sup- 
pi  v  nutritive  elements  to  nervous  system  by  proper  food,  prop- 
erly digested  ;  by  increasing  circulatory  power  ;  by  exercise  ;  by 
hydrotherapy  ;  by  massage  ;  and  diminish  expenditure  of  nervous 
energy  by  rest,  if  necessary  absolute,  and  by  diversion. 

Direct  treatment  may  be  by  tonics  of  all  kinds  ;  by  sedatives, 
if  patient  is  extremely  nervous  ;  by  electricity  ;  galvanism. 
Treat  symptoms  only  when  absolutely  necessary.  Combat  the 
desire  of  these  patients  for  drugs,  and  their  dependence  on  stimu- 
lants and  opiates. 

HYSTERIA. 

A  functional  disturbance  of  the  nervous  system  characterized 
by  mental  and  moral  perversion,  lack  of  self-control  and  disor- 
ders of  any  or  all  of  the  bodily  functions. 

Women,  between  fifteen  and  twenty-five  years,  or  at  any  age. 

Men,  at  any  age,  and  even  children,  may  be  affected. 

Causes. — Hereditary  influence  very  marked  ;  malnutrition  of 
the  nervous  system  from  anaemia  ;  indigestion  ;  from  bad  habits 
of  life  ;  emotional  excitement ;  fear,  anxiety,  jealousy ;  tendency 
to  imitation  yielded  to  ;  epidemics  of  hysteria  ;  uterine  and  ova- 
rian irritation  is  a  rare  cause.  Traumatism,  especially  accidents 
attended  by  great  fear.  Several  causes  may  concur. 

Symptoms, — i.   Mental  changes,  and  moral  perversion. 

Increased  irritability,  and  emotional  excitability  with  impaired 
self-control. 

Excessive  emotion  leads  to  exhaustion. 

Craving  for  notice  and  sympathy. 

All  sorts  of  means  taken.  Self-injury;  sores  which  won't 
heal ;  needles  swallowed  ;  blood  sucked  and  vomited  ;  animals 
concealed. 

Purposeless  acts  of  criminal  kind,  like  reasoning  mania. 


74  DISEASES   OF   THE   NERVOUS   SYSTEM. 

Hallucinations  may  occur. 

Depression  is  not  uncommon,  and  melancholia  may  be 
feared.  But  in  melancholia  facial  expression  is  characteristic, 
thought  is  slow,  delusions  are  of  self-accusation,  weight  is  rapidly 
lost. 

2.  Disorders  of  various  functions  : 

(1)  Motor. — Spasms,  contractures,  paralysis,  convulsions,  glo- 
bus  hystericus,  vomiting,  diarrhoea,  vesical  irritation,  convulsion 
attended  by  sobbing  and   crying,  lasts  longer  than  an  epileptic- 
fit,  does  not  begin  or  end  suddenly,  and  tongue  is  not  bitten,  and 
there  is  no  asphyxia.     Paralysis,  varies  in  intensity,  does  not  af- 
fect the  face   in  hemiplegia,  no  typical  gait,  no  bed-sore,  no  in- 
continence ;  aphonia,  aphasia,  cough. 

(2)  Sensory. — Hyperaesthesia  of  special  senses,  dislike  of  light 
or  noises  ;  hyperaesthesia  of  skin,  spinal  irritation  ;  hyperaesthe- 
sia  of  limbs,  numbness  ;  hyperaesthesia  of  ribs,  pressure  of  dress  ; 
hyperaesthesia   of   ovaries ;  hyperaesthesia   of   bladder,  frequent 
micturition  ;  pain  anywhere,  rarely  definitely  localized  ;  especially 
in  joints,  hip,  knee,  ankle,  wrist,  elbow  ;  fixation,  atrophy  of  mus- 
cles ;  joints  easily  moved  under  ether  ;  no  deformity  ;  anaesthe- 
sia to  pain,  usually  localized,  in  skin  or  mucous  membranes  ;  uni- 
lateral loss  of  special  senses. 

(3)  Vaso-motor. — Palpitation  and  faints ;  variations  of  arterial 
tone,  flashes,  oedema  ;  hematemesis,   haemoptysis  ;  small  hemor- 
rhagic  spots,  stigmata  ;  rises  of  temperature,  105°  to  110°  F. 

(4)  Secretion. — Saliva  ;  gastric  juice  varies.     Urine  —  or  +. 

Hysterical  attacks  :  Crying  and  laughing,  produced  by  emo- 
tional strain  ;  scream,  convulsion,  opisthotonus,  facial  expression, 
series  of  short  attacks,  fit  of  crying,  passes  water,  cataleptic 
rigidity,  hystero-epilepsy. 

The  character  of  the  symptoms  varies  greatly.  The  symptoms 
appear  and  disappear  suddenly. 

The  course  of  the  disease  :  Chronic  condition  with  periods  of 
intensity ;  cure,  sudden  and  marvellous  ;  great  variation  in 
symptoms  ;  very  rarely  death  in  convulsion  or  from  suicide. 

Diagnosis  is  never  made  from  a  single  symptom  but  from  a 
study  of  the  general  condition. 

Treatment. — Mental  change  and  moral  education  ;  hydrother- 
apy  ;  the  rest  cure  ;  mental  therapeutics  ;  tonics,  strychnine,  iron 
and  quinine. 

Symptomatic  remedies : 


DISEASES    OF   THE   NERVOUS   SYSTEM.  75 

Sedatives  for  the  nervous  state,  bromides,  valerian,  lavender, 
asafoetida.  Opium  is  to  be  avoided,  for  habit  is  easily  formed. 

For  convulsion,  prevent  injury,  don't  use  chloroform,  use 
cold  water,  hold  patient,  stop  respiration,  don't  press  ovaries, 
give  emetic. 

For  faints,  irritation  over  heart  by  ice,  internally  spirits  am- 
monia, or  lavender. 

For  spasms,  hot  or  cold  applications,  cautery. 

For  paralysis,  electricity,  especially  faradism. 

For  pain,  hypodermics  of  water  after  one  of  morphine,  local 
applications  of  sedatives. 


1.— Normal  Nerve  Fibre,    a,  Axis  cylinder;  6,  medullary  sheath;  c,  sheath  of  Kchwann;  d,  node  of  Ranvw 
e,  incisure  of  Schmidt;  /,  nucleus  of  sheath  of  Scliwann. 


•  - "~ " 


Fra.  '<}.  -Degeneration  of  Nerve  Fibres  in  Various  Stages. 


FIG.  3. -Cross  Section  of  Normal  and  Degenerated  Nerve  Trunk. 
1 


I  C 


Fio.  4. — The  Spinal  Cord  with  its  Nerves  (Anterior  Sur- 
;e).  Brachial,  Lumbar,  and  Sacral  Plexuses  and  Nerves 
Extremities  shown  on  left:  Sympathetic  Ganglia  with  Spi- 
1  Roots  shown  on  right  of  the  figure. 


FIG.  5.— The  Relation  of  the  Spinal  Con 
the  Vertebral  Bodies  and  Spines.  The  0 
ends  at  L.  I. 


FIG.  6. — Diagram  of  a  Spinal  Segment  as  a  Spinal  Centre 
and  as  a  Conducting  Medium  (Bramwell).  B,  Right;  B',  left 
hemisphere  ;  MO,  medulla  oblongata  ;  1,  motor  tract  from 
right  hemisphere;  at  MO  it  divides  into  a  direct  and  a  crossed 
tract,  the  former  passes  down  the  right  ant.  median  column, 
the  latter  passes  down  the  left  lateral  column,  giving  off  at  1' 
fibres  to  the  ant.  gray  horns  of  the  cord,  in  which  the  motor 
cells  lie,  from  which  nerves  pass  to  muscles,  M;  2,  motor 
tract  from  left  hemisphere;  S,  S',  sensitive  areas  on  the  left 
side  of  the  body;  3.  3',  the  main  sensory  tract  from  the  left 
side  of  the  body;  it  passes  into  the  post,  gray  matter  of  the 
segment,  then  decussates,  and  passes  up  the  right  half  of  the 
cord  in  the  post,  columns,  thence  to  the  right  hemisphere  of 
the  brain;  4,  4',  the  main  sensory  tract  from  the  right  side  of 
the  body;  5,  6,  the  tracts  of  muscular  sense  from  the  legs, 
passing  up  upon  the  same  side  of  the  spinal  cord  in  which  it 
enters,  in  the  column  of  Goll,  decussating  at  the  medulla, 
above  the  motor  decussation.  The  arrows  indicate  the  direc- 
tion of  nerve  currents. 


Fio.  7.— Diagram  of  a  Section  of  the  Spinal  Cord  in  the  Cervical  Region.  A.C.,  Ant.  commissure;  P.O., 
)st.  commissure;  I.g.s.,  intermediate  gray  substance;  P.Cor.,  post,  comu;  c.c.p.,  caput  cornu  post. ;  L.L.L., 
teral  limiting  layer;  AL-AT.,  antero-lateral  ascending  tract. 

3 


C.  II. 


D.  VIII. 


C.  V. 


D.  XII. 


C.  VII. 


I,.  II. 


D.  I. 


L.  IV. 


S.  I. 


FIG.  8.— Sections  of  Spinal  Cord.  1  to  6,  Groups  of  cells  in  ant.  horns.  I.-IX..  Columns  of  cord.  I.,  Ant. 
median.  //.,  Anterior.  III.,  Antero-lateral.  TV.;  Lateral  pyramidal.  V..  Lateral  limiting:  layer.  VI.,  Pos- 
tero-lateral  or  Burdach.  VII.,  Postero-median  or  Goll.  VIII.,  Ant.-lateral  ascending.  IX.,  Direct  cere- 
bellar.  Between  IV.  and  VI.,  Col.  of  Lassauer. 


liv 


FIG.  9. — The  Base  of  the  Brain  and  the  Cranial  Nerves. 
ra,  Pons  and  Medulla  (Allen  Thompson).  I.  to  XII.,  The 
aial  nerves;  Th,  optic  thalamus;  h,  pituitary  body;  tc, 
3r  cinerium;  a,  corpora  albicantia;  P,  pes  pedunculi;  i, 
rior,  and  e,  exterior,  geniculate  body;  PV,  pons  Varolii; 
anterior  pyramid  of  medulla;  o,  olive;  d,  decussation  of 
erior  pyramids;  ca,  anterior  column  of  spinal  cord;  cJ, 
ral  column  of  spinal  cord;  Ce,  cerebellum:  fl,  flocculus  of 
sbellum. 


FIG.  10.— Side  View  of  Pons  and  Medulla  to 
show  Nuclei  and  Roots  of  Cranial  Nerves.  V.- 
XII. ,  nuclei ;  KV.-VII..  roots  of  nerves;  V,  long 
ascending-  nucleus  of  V. ;  O,  olive;Os,  supe- 
rior olivary  body;  Gf,  knee  of  facial  nerve  root. 


FIG.  11.— The  Motor  Tract  in  the  Cms,  Pons,  and 
Medulla.  A,  Lesion  causes  hemiplegia.  B,  Lesion 
causes  alternating  paralysis;  left  facial,  right 
extremities.  C,  Lesion  causes  paralysis  of  limbs 
and  tongue.  D,  Lesion  causes  paralysis  of  limbs 
of  opposite  side.  E,  Lesion  in  motor  decussation 
causes  bilateral  paralysis. 


FIG.  12. — The  Sensory  Tract  in  the  Crus,  Pons 
and  Medulla,  showing  Nucleus  and  Roots  of  V 
Nerve.  A,  Lesion  causes  hemianaesthesia.  B,  Le 
sion  causes  alternating  hemianaesthesia;  left  fa« 
and  right  side  of  body. 


•YL 


FIG.  13.— Sagittal  Section  through  the  Cerebral  Axis  to  show  the  Nuclei  of  the  Ocular  Nerves 
in  the  Floor  of  the  Aqueduct  of  Sylvius  and  Fourth  Ventricle  and  the  Course  of  the  Nerves  to 
their  Exit.  The  various  groups  of  cells  from  which  the  III.  N  arises  are  seen.  RN,  Red  nucleus 
of  tegmentum ;  L,  lemniscus  (sensory  tract) ;  CC,  motor  tract  in  the  cms  cerebri  seen  to  traverse 
the  pons  and  enter  the  ant.  pyramid  of  tbe  medulla. 


FIQ.  14.— The  Lateral  Surface  of  the  Left  Hemisphere  (Eberstaller).  S,  Fissure  of  Sylvius;  C,  fissure  of 
Rolando,  or  central  fissure;  pel,  sulcus  prse-centralis  inferior;  pcs,  "sulcus  praecentralis  superior;  r(c,  ^sulcus 
retro-centralis;  sfr,  sulcus  sub-frontalis;  fl,f2,  /3,  sulcus  frontalis,  sup.,  inf.  et  medius;  ip,  interparietal  ^fls- 
sure;  po,  parieto-occipital  fissure;  occ.  ant.,  occ.  lat.,  fissure,  occipitalis,  ant.  et  lat. ;  tl,  to,  t'i,  sulci^temporales; 
A,  B,  ant.  and  post,  central  convolutions;  -Pi,  F£,  Ft,  frontal  convolutions,  sup.,  med.,  inf.;  PI,  P2,~parietal 
convolutions,  sup.  and  inf.;  G.  spm,  gyrus  supra-marginalis;  G.  ang,  gyrus  angularis;  0,  occipital  lobe;  21, 
T2,  TS,  temporal  convolutions. 


FIG.  15.— The  Functional  Areas  of  the  Brain,  Left  Hemisphere. 


,XP° 


FIG.  16.— The  Median  Surface  of  the  Right  Hemisphere  (after  Ecker).  The  visual  centre  is  in  the  cortex 
lying  kwithin[the  calcarine  fissure,  OC,  and  in  the  cuneus,  Oz.  The  sensations  of  smell  and  taste  are 
received  in  the  uncinate  convolution,  V,  and  at  the  tip  o'f  the  temporo-sphenoidal  lobe.  A,  B  shows  the  posi- 
tion of  the'paracentral  lobule,  which  is  included  in  the  motor  area  of  the  leg. 


FIG.  17. — The  Association  Fibres.  A,  Between  adjacent  convolutions;  B,  between  frontal  and  occipital 
areas;  C,  between  frontal  and  temporal  areas,  cingulum;  D,  between  frontal  and  temporal  areas,  fasciculus 
uncinatus  ;  E,  between  occipital  and  temporal  areas,  fasciculus  longitudinalis  inferior;  CN,  caudate  nucleus; 
OT,  optic  thalamus. 


FIG.  18.— The  Projection  Tracts  joining  the  Cortex  with  Lower  Nerve  Centres.  Sagittal  section  showing 
the  arrangement  of  tracts  in  the  internal  capsule.  A,  Tract  from  the  frontal  lobe  to  the  pons,  thence  to  the 
cerebellar  hemisphere  of  the  opposite  side;  B,  motor  tract  from  the  central  convolutions  to  the  facial  nucleus 
in  the  pons  and  to  the  spinal  cord;  its  decussation  is  indicated  at  K;  C,  sensory  tract  from  posterior  columns 
of  the  cord,  through  the  posterior  part  of  the  medulla,  pons,  crus,  and  capsule  to  the  parietal  lobe ;  D,  visual 
tract  from  the  optic  thalamus  (OT)  to  the  occipital  lobe;  E,  auditory  tract  from  the  inter-geniculate  body,  to 
which  a  tract  passes  from  the  VIII.  N.  nucleus  (J)  to  the  temporal  lobe;  F,  superior  cerebellar  peduncle;  G, 
middle  cerebellar  peduncle;  H,  inferior  cerebellar  peduncle;  CN,  caudate  nucleus;  CQ,  corpora  quadrige- 
mina ;  Vt,  fourth  ventricle.  The  numerals  refer  to  the  cranial  nerves. 


FIG.  19.— Horizontal  Section  through  Right  Hemisphere  showing  the  Internal  Capsule  and  Basal  Ganglia. 
F,  Fornix;  NO,  caudate  nucleus;  OT,  optic  thalamus:  NL,  lenticular  nucleus;  IR,  island  of  Reil;  EC, 
external  capsule;  V,  lateral  ventricle;  1C,  int.  capsule,  ant.  part;  Fa,  facial  tract;  M,  motor  tract  to  limbs; 
S.  sensory  tract:  O,  visual  tract,  all  in  the  post,  part  of  the  capsule. 


Fio.  20.— The  Motor  Tract.  S,  Fissure  of  {Sylvius;  NL,  lenticular  nucleus;  OT,  optic  thalamus;  NO,  cau- 
date nucleus;  C,  eras;  P,  pons;  M,  medulla;  O,  olivary  body.  The  tracts  for  face,  arm,  and  leg  gather  from 
the  lower,  middle  and  upper  thirds  of  the  motor  area,  pass  into  the  capsule  and  through  the  crus  and  pons, 
where  the  face  fibres  cross  to  the  opposite  VII.  N.  nucleus,  while  the  others  pass  on  to  the  lower  medulla, 
where  they  partially  decussate  to  enter  the  lateral  column  of  the  cord,  the  non-decussating  fibres  passing 
into  the  ant.  median  columns.  Lesion  in  cortex  causes  monoplegia ;  in  capsule,  hemi plegia ;  in  pons,  alternating 
paralysis. 


10 


& 


FIG.  21. — The  Visual  Tract.  The  result  of  a  lesion  anywhere  between  the  chiasm  and  the  cuneus  is  to 
produce  homonymous  hemianopsia.  H,  Lesion  at  chiasm  causing  bilateral  temporal  hemianopsia;  N,  lesion 
at  chiasm  causing  unilateral  nasal  hemianopsia;  T,  lesion  at  chiasm  causing  unilateral  temporal  hemianop- 
sia; SN,  substantia  nigra  of  cms;  L,  lemniscus  in  crus;  RN,  red  nucleus;  1/7.  third  nerves. 


FIG.  22. — Diagram  to  illustrate  the  Concept  "Bell" 
and  to  show  the  Varieties  of  Apraxia  and  Aphasia.  The 
memory  pictures  are  relics  of  past  perceptions  received 
through  different  senses.  The  association  makes  up  the 
mental  image  bell.  The  word  image  is  made  up  of  the 
memories  of  the  sound  and  appearance  of  the  word,  and 
of  the  uttering  and  writing  effort  memories;  these  are 
joined  together.  The  mental  image  and  the  word  image 
are  also  joined  with  one  another,  making  up  the  con- 
cept "bell." 


GfabfHa 


FIG.  23.— Diagram  to  show  the  Relation  of  the  Skull  and  its  Sutures  to  the  Fissures  of  Rolando  and  Sylvius. 

12 


FIG.  24. — Photograph  of  Model  of  Head,  showing  Relation  of  Cranial  Sutures  to  the  Convolutions  of  the 
brain.  R,  Fissure  of  Rolando;  J,  inter  parietal  fissure;  PO,  parieto-occipital  fissure;  S,  fissure  of  Sylvius: 
F.  frontal;  P,  parietal:  O,  occipital:  T.  temporal  lobes;  A,  ant.  cent.,  and  P.  post.  cent,  convolution. 


fr, 


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